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At least 19 recordsLinked to original sources

PubMed2000

The roles of orthostatic hypotension, orthostatic tachycardia, and subnormal erythrocyte volume in the pathogenesis of the chronic fatigue syndrome.

BACKGROUND: Orthostatic hypotension during upright tilt is an important physical disorder in patients with chronic fatigue syndrome. We have tested its occurrence during prolonged standing, whether it is correctable, and whether reduced circulating erythrocyte volume is present. METHODS: Fifteen patients were randomly selected from a large population of patients with chronic fatigue syndrome, studied, and observed for several years (by DSB). Blood pressure (BP) and heart rate (HR) measured with Dinamap every minute for 30 minutes supine and 60 minutes standing were compared with these findings in 15 healthy age- and gender-matched control subjects and later during lower body compression with military antishock trousers (MAST). Plasma catecholamines and circulating erythrocyte and plasma volumes were also measured by isotopic dilution methods. RESULTS: Abnormal findings in the patients included excessive orthostatic reductions in systolic (P < 0.001) and diastolic BP (P < 0.001) and excessive orthostatic tachycardia (P < 0.01), together with presyncopal symptoms in 11 of the 15 patients and in none of the control subjects after standing for 60 min. Lower body compression with the MAST restored all orthostatic measurements to normal and overcame presyncopal symptoms within 10 min. Circulating erythrocyte but not plasma volumes were subnormal in the 12 women (P < 0.01) and plasma norepinephrine concentration rose excessively after standing for 10 min. CONCLUSION: Delayed orthostatic hypotension and/or tachycardia caused by excessive gravitational venous pooling, which is correctable with external lower-body compression, together with subnormal circulating erythrocyte volume, are very frequent, although not invariably demonstrable, findings in moderate to severe chronic fatigue syndrome. When present, they may be involved in its pathogenesis.

Adolescent↗

PubMed2003

Orthostatic hypotension.

Orthostatic hypotension is a physical finding defined by the American Autonomic Society and the American Academy of Neurology as a systolic blood pressure decrease of at least 20 mm Hg or a diastolic blood pressure decrease of at least 10 mm Hg within three minutes of standing. The condition, which may be symptomatic or asymptomatic, is encountered commonly in family medicine. In healthy persons, muscle contraction increases venous return of blood to the heart through one-way valves that prevent blood from pooling in dependent parts of the body. The autonomic nervous system responds to changes in position by constricting veins and arteries and increasing heart rate and cardiac contractility. When these mechanisms are faulty or if the patient is hypovolemic, orthostatic hypotension may occur. In persons with orthostatic hypotension, gravitational opposition to venous return causes a decrease in blood pressure and threatens cerebral ischemia. Several potential causes of orthostatic hypotension include medications; non-neurogenic causes such as impaired venous return, hypovolemia, and cardiac insufficiency; and neurogenic causes such as multisystem atrophy and diabetic neuropathy. Treatment generally is aimed at the underlying cause, and a variety of pharmacologic or nonpharmacologic treatments may relieve symptoms.

Diagnosis, Differential↗

PubMedDate not supplied

Diagnosis and treatment of supine hypertension in autonomic failure patients with orthostatic hypotension.

Orthostatic hypotension is seen in various medical conditions. It can be secondary to medications or volume depletion. It can also be due to autonomic neuropathy secondary to other diseases, such as diabetes mellitus, or to primary degenerative processes of the autonomic nervous system. Orthostatic hypotension dominates the clinical picture of patients suffering from autonomic failure. Paradoxically, about one half of these patients also suffer from supine hypertension, which induces pressure natriuresis, worsening orthostatic hypotension. It also complicates the treatment of orthostatic hypotension. Supine hypertension is mediated by an increase in peripheral vascular resistance. This is due to residual sympathetic tone in patients with multiple system atrophy (Shy-Drager syndrome), but the cause is not known in patients with pure autonomic failure, who have increased vascular resistance despite very low levels or plasma norepinephrine and renin activity. The recent observation that patients with supine hypertension develop left ventricular hypertrophy suggests they should be treated. During the day, avoiding the supine position is often all that is required. Short-acting vasodilators (e.g., transdermal nitroglycerin) can be used during the night.

Antihypertensive Agents↗

PubMed1997

Evaluation and treatment of orthostatic hypotension.

Orthostatic hypotension is defined as a decrease of at least 20 mm Hg in systolic blood pressure when an individual moves from a supine position to a standing position. Nonneurogenic causes of orthostatic hypotension are related to cardiac pump failure, reduced intravascular volume, venous pooling or a medication side effect. Neurogenic causes include both central and peripheral nervous system lesions. The diagnostic evaluation requires a systematic review of medications and coexisting medical conditions along with a neurologic examination to search for treatable factors that may be contributing to orthostatic hypotension. Specific testing of autonomic function is useful for detecting subclinical orthostatic hypotension or for monitoring autonomic function over a period of time. Treatment is directed at improving the patient's symptoms rather than achieving arbitrary blood pressure goals.

Humans↗

PubMed1988

Sodium chloride treatment of antidepressant-induced orthostatic hypotension.

Orthostatic hypotension, a serious, frequent side effect of antidepressant medication, can be severe enough to require cessation of medication. The authors report three cases of antidepressant-induced orthostatic hypotension treated with sodium chloride. In two of the cases, the use of sodium chloride allowed the patient to continue antidepressant treatment at a therapeutically effective dosage. The authors discuss risks and treatment of orthostatic hypotension.

Adolescent↗

PubMed1990

Diversity in supercoupling of beta 2-adrenergic receptors in orthostatic hypotension.

Orthostatic hypotension is a clinical condition that frequently involves abnormal adrenergic control of cardiovascular function. Adrenergic function was studied in six patients with symptomatic orthostatic hypotension and in 11 age-matched healthy subjects. The patients demonstrated higher supine mean arterial pressures (MAP; 103 +/- 8 versus 86 +/- 4 mm Hg) and orthostatic hypotension (delta MAP -70 +/- 5 versus +15 +/- 2 mm Hg, p less than 0.001) compared with normal subjects. The delta MAP in phase II of the Valsalva maneuver was significantly greater (-31 +/- 4 versus -7 +/- 4 mm Hg, p less than 0.002) and phase IV heart rate response was blunted (-5 +/- 3 versus -30 +/- 8 beats/min, p less than 0.02) in these patients. More isoproterenol was required to increase heart rate by 25 beats per minute in patients with hypotension (810 +/- 670 versus 3.1 +/- 1.3 micrograms, p less than 0.05), indicating marked chronotropic hyposensitivity. Leukocyte beta 2-adrenergic receptor densities were similar in patients and controls. beta 2-Adrenergic receptor coupling, however, was elevated in patients with hypotension when compared with control subjects (ratio of the low-affinity and high-affinity dissociation constants [KL/KH] 140 +/- 7.4 versus 66 +/- 4.3, p less than 0.001). There were negative correlations between the KL/KH value and the dose of isoproterenol required to decrease MAP by 20 torr (p less than 0.02) and between the KL/KH value and the product of the hormone receptor and MAP (p less than 0.01). However, the patients could be subdivided into a group who could mount a nearly normal hormone receptor times MAP response on standing (group 1A), and a group who could not (group 1B). The group 1A patients had elevated plasma norepinephrine responses associated with milder beta 2-adrenergic receptor supercoupling, whereas group 1B patients had essentially no orthostatic plasma norepinephrine response and had much higher KL/KH values. Thus, though a state of biochemical supersensitivity existed in both patient subgroups, diminished catecholamine exposure was associated, as expected, with beta 2-adrenergic hypersensitivity in group 1B, whereas there was no diminution of catecholamine exposure in the beta 2-adrenergic hypersensitivity observed in group 1A patients.

Aged↗

PubMed1985

Gastrointestinal motility disturbances in patients with orthostatic hypotension.

Orthostatic hypotension syndromes may be associated with visceral denervation, resulting in disturbances of the gastrointestinal and urinary systems. This report analyzes the findings in 9 patients with neurogenic orthostatic hypotension and gastrointestinal symptoms. Antral and proximal small intestinal motor dysfunction was demonstrated in all patients: a significant reduction (p = 0.007) in the number of interdigestive motor complexes during 3 h of fasting (mean 0.4 vs. 1.3 controls); absence of gastric component in interdigestive motor complexes observed; incoordination of fasting and fed antral activity; and development of nonpropagating bursts of phase III-like activity in the intestine that were of at least 2-min duration, high amplitude and frequency, and associated with tonic elevations in baseline pressure. These motor abnormalities may provide a potential means for the diagnosis of impaired autonomic supply to the upper gut.

Adult↗

PubMed1992

[Methods of investigating orthostatic hypotension].

Orthostatic hypotension, which is common mainly in the elderly, is in many cases related to hypovolemia and/or vasodilators intake. However, when an impairment of the autonomic nervous system is suspected, orthostatic hypotension severity and mechanism may be investigated. The most common tests are the head upright tilt-test and the Valsalva manoeuvre. Both of them examine the baroreflex system as a whole, and become non invasive tests with the development of finger arterial blood pressure continuous measurement. Each part of the baroreflex system may be investigated separately. So, cardiac vagal responses to ocular compression, to carotid sinus massage, to respiratory change or to atropine infusion, may be tested. On the other hand, sympathetic efferent pathways may be stimulated in a variety of ways, such as isometric exercise, cutaneous cold, mental arithmetic, norepinephrine infusion, or tiltest. None of these tests should be applied systematically, but according to the clinical features.

Aged↗

PubMed1995

Recent advances in the treatment of orthostatic hypotension.

Orthostatic hypotension is a fall in blood pressure on standing that causes symptoms of dizziness, visual changes, and discomfort in the head and neck. The goal of treatment is the improvement of the patient's functional capacity, rather than a target blood pressure. For treatment to be successful, it must be individualized. Non-pharmalogic interventions include carefully managed exercise, scheduled activities, and monitoring of the environmental temperature. Agents such as fludrocortisone, midodrine, and epoetin alfa offer successful pharmacologic interventions. Although these measures ease the symptoms of orthostatic hypotension, current approaches neither reverse nor stabilize the disease process in autonomic disorders.

Humans↗

PubMed2003

Treatment of orthostatic hypotension.

Orthostatic hypotension is the most incapacitating symptom of autonomic failure. This disorder occurs with both central autonomic neurodegenerative disorders, such as multiple system atrophy and Parkinson's disease, and peripheral autonomic disorders, such as the autonomic peripheral neuropathies and pure autonomic failure. The hallmark of both central and peripheral causes of neurogenic orthostatic hypotension is the failure to release norepinephrine appropriately upon standing. Patient education is the cornerstone of management. There are several measures that can be implemented to improve orthostatic tolerance prior to pharmacological intervention. Plasma volume expansion is essential to improve orthostatic tolerance, and fluid and sodium chloride intake should be increased. Most patients can be treated successfully with volume expansion or fludrocortisone or both in combination with a sympathomimetic agent. Desmopressin acetate and erythropoietin are useful supplementary agents in patients with more refractory symptoms. There are rare patients who will require additional agents to treat their symptoms. A small group of patients remain refractory to all therapeutic modalities.

Animals↗

PubMed2006

Insular pathology in Parkinson's disease patients with orthostatic hypotension.

Orthostatic hypotension (OH) in Parkinson's disease (PD) patients may be a significant source of morbidity and discomfort. Although peripheral ANS components have been associated with its development, central mechanisms are probably involved. The insular cortex is a central site of autonomic and limbic integration and neuropathologic studies have indicated its involvement in the neurodegenerative process of PD. To this end, we studied the neuropathology of the insular, temporal and parietal cortices in PD patients with and without OH. Our results suggest an association between the severity of PD-related neuropathology in the insular cortex and OH. Further research into the subject is warranted.

Age of Onset↗

PubMed1989

Orthostatic hypotension.

Orthostatic hypotension is a rare finding in healthy elderly subjects, but is a common clinical problem in older patients. Assessment of symptoms and the blood pressure response to standing is an important part of the initial evaluation and follow-up of geriatric patients. Generally, more than one cause will be identified, and these patients respond to simple treatment measures. Identification and treatment of this disorder will improve function and independence in this population.

Aged↗

PubMed2002

Treatment of orthostatic hypotension.

Orthostatic hypotension (OH) is a fall in blood pressure after assuming an upright position. Whereas asymptomatic patients usually need no treatment, the majority of symptomatic patients can be cured by avoidance of trigger mechanisms and the use of physical countermaneuvers and non-pharmacological interventions. Several pharmacological therapies are available and generally fludrocortisone and midodrine are the drugs of first choice. Recently, highly individualized therapy with ambulatory norepinephrine therapy was able to mobilize otherwise immobile patients.

Cardiovascular Agents↗

PubMed2006

Sodium paradoxically reduces the gastropressor response in patients with orthostatic hypotension.

Orthostatic hypotension (OH) can cause syncope that is difficult to treat. We have found that 473 mL (16 oz) of water can increase systolic blood pressure (SBP) by > 30 mm Hg in many OH patients (the gastropressor response). OH patients are routinely advised to increase their sodium intake to augment their blood volume. We tested the hypothesis that the ingestion of salt with water would increase the magnitude of the acute pressor response compared with water alone in patients with OH. Patients with OH (n = 9; female = 5; 65+/-3 years) underwent a randomized crossover trial of drinking water (H2O) and salt water (NaCl-H2O). Noninvasive heart rate and BP were measured with the patient seated for > or = 60 minutes after ingestion. The area under the curve for SBP was greater with H2O than NaCl-H2O for the 30 minutes (714+/-388 mm Hg x min versus 364+/-369 mm Hg x min; P = 0.002) and 60 minutes (1454+/-827 mm Hg x min versus 812+/-734 mm Hg x min; P = 0.048) after ingestion. The increase in SBP with H2O was greater than with NaCl-H2O at 30 minutes (37+/-6 versus 18+/-5 mm Hg; P = 0.006) but not at 60 minutes (17+/-6 versus 10+/-6 mm Hg; P = 0.4). Norepinephrine increased after H2O (P = 0.018) but not after NaCl-H2O (P = 0.195). Both oral water and salt water increase BP in patients with OH. Instead of augmenting the gastropressor response, the additional salt paradoxically attenuates the pressor response to water. These data suggest a potentially important role for gastrointestinal osmolality in the activation of the sympathetic nervous system leading to cardiovascular reflexes responsible for the gastropressor response.

Aged↗

PubMed1992

[Etiological aspects of orthostatic hypotension].

Orthostatic hypotension (OH) must be distinguished from supine hypotension made worse by standing up and, in particular, from vasovagal syncope. At first approximation, asympathicotonic invariable pulse OH virtually always related to an organic lesion of the baroreflex arch must be distinguished from variable pulse OH which is usually functional and may also be due to organic lesions with exclusive or predominant sympathetic system disorders. In case of doubt, it may be useful to measure palmar and plantar sympathetic potentials. The principal causes of variable pulse OH are therapeutic drugs, absolute or relative hypovolaemia, endocrine diseases (adrenal insufficiency, phaeochromocytoma), spinal quadriplegia and two congenital diseases including dopamine beta-hydroxylase deficiency. In Guillain-Barré syndrome, diabetes and alcoholism, the OH pulse may be variable or invariable. The main causes of asympathicotonic OH are ageing, post-prandial period, certain infections (e.g. tabetic neurosyphilis, botulism, EBV and HIV infections), a few systemic diseases and isolated neurological diseases. Among the systemic diseases responsible for OH are diabetes, alcoholism and chronic liver diseases of other causes, porphyria, lead poisoning, Biermer's disease, amyloidosis, several connective tissue diseases, including systemic lupus erythematosus, and some cancers associated or not with Lambert-Eaton syndrome. Among isolated neurological diseases are the familial diseases described by Riley and Day, multisystem atrophies (first described by Shy and Dager) and pure peripheral dysautonomia. To differentiate the latter from an incipient Shy-Dager syndrome, it may be helpful to use pharmacological tests: plasma catecholamine levels measurements in supine position, and clonidine test with repeated growth hormone assays in upright position.

Blood Pressure Determination↗

PubMed1988

Orthostatic hypotension.

Orthostatic hypotension is a potentially debilitating condition in the elderly. It may be associated with aging, drug therapy or underlying disease. Pathophysiologic mechanisms can be classified as vasovagal, sympathicotonic and asympathicotonic (autonomic nervous system disease). Only a detailed history will uncover the disorder in some patients. When conservative measures fail, fludrocortisone is a generally helpful drug that induces volume expansion.

Aged↗

PubMed2005

Should we screen hospice inpatients for orthostatic hypotension?

Orthostatic hypotension (OH) is defined as a reduction in systolic blood pressure of at least 20 mm Hg or a reduction in diastolic blood pressure of at least 10 mm Hg within three minutes of standing, with a reported prevalence of 40% in the hospice setting. Dizziness, falls and fractures have been attributed to OH and some cases of symptomatic OH might be reversible. This study explored the case for screening hospice inpatients for OH. Fifty-nine patients were screened up to five times and, whilst the detection rate was 27%, in no case was it reproducible. There was no statistical association between orthostatic symptoms and the detection of OH, and no patients benefited from the screening process. On closer examination of the literature, the current definition of OH might benefit from revision, sphygmomanometry is an unsatisfactory screening method and there is currently no case for screening hospice inpatients for OH.

Adult↗

PubMed1997

Efficacy of compression of different capacitance beds in the amelioration of orthostatic hypotension.

Orthostatic hypotension (OH) is the most disabling and serious manifestation of adrenergic failure, occurring in the autonomic neuropathies, pure autonomic failure (PAF) and multiple system atrophy (MSA). No specific treatment is currently available for most etiologies of OH. A reduction in venous capacity, secondary to some physical counter maneuvers (e.g., squatting or leg crossing), or the use of compressive garments, can ameliorate OH. However, there is little information on the differential efficacy, or the mechanisms of improvement, engendered by compression of specific capacitance beds. We therefore evaluated the efficacy of compression of specific compartments (calves, thighs, low abdomen, calves and thighs, and all compartments combined), using a modified antigravity suit, on the end-points of orthostatic blood pressure, and symptoms of orthostatic intolerance. Fourteen patients (PAF, n = 9; MSA, n = 3; diabetic autonomic neuropathy, n = 2; five males and nine females) with clinical OH were studied. The mean age was 62 years (range 31-78). The mean +/- SEM orthostatic systolic blood pressure when all compartments were compressed was 115.9 +/- 7.4 mmHg, significantly improved (p < 0.001) over the head-up tilt value without compression of 89.6 +/- 7.0 mmHg. The abdomen was the only single compartment whose compression significantly reduced OH (p < 0.005). There was a significant increase of peripheral resistance index (PRI) with compression of abdomen (p < 0.001) or all compartments (p < 0.001); end-diastolic index and cardiac index did not change. We conclude that denervation increases vascular capacity, and that venous compression improves OH by reducing this capacity and increasing PRI. Compression of all compartments is the most efficacious, followed by abdominal compression, whereas leg compression alone was less effective, presumably reflecting the large capacity of the abdomen relative to the legs.

Adult↗