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PubMed · 6710110

[Orthostatic hypotension].

P Weidmann
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Abstract

The practicing physician commonly encounters patients with hypotensive disturbances of orthostatic blood pressure regulation. These include the functional orthostatic syndrome as well as the true forms of orthostatic hypotension due to hypovolemia, certain cardiac, pulmonary or endocrine diseases, or (particularly in the elderly) autonomic dysfunction of varying etiology. The possible pathogenetic mechanisms are also many and varied, while various drugs may play a causative or contributory role. Careful evaluation and treatment with general measures and, if indicated, pharmacologic agents may (even in the presence of severe neurogenic orthostatic hypotension) often lead to marked improvement in blood pressure and in quality of life.

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Autonomic Nervous System DiseasesBlood VolumeCardiovascular DiseasesDiagnosis, DifferentialEndocrine System DiseasesHemodynamicsHumansHyponatremiaHypotension, OrthostaticPostureSyncopeEnglish AbstractJournal Article

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P Weidmann. 1984-02-25. [Orthostatic hypotension].. https://pubmed.ncbi.nlm.nih.gov/6710110/

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PubMed2006

Cardiovascular and cerebrovascular responses to lower body negative pressure in type 2 diabetic patients.

In diabetic patients, vascular disease and autonomic dysfunction might compromise cerebral autoregulation and contribute to orthostatic intolerance. The aim of our study was to determine whether impaired cerebral autoregulation contributes to orthostatic intolerance during lower body negative pressure in diabetic patients. Thirteen patients with early-stage type 2 diabetes were studied. We continuously recorded RR-interval, mean blood pressure and mean middle cerebral artery blood flow velocity at rest and during lower body negative pressure applied at -20 and -40 mm Hg. Spectral powers of RR-interval, blood pressure and cerebral blood flow velocity were analyzed in the sympathetically mediated low (LF: 0.04-0.15 Hz) and the high (HF: 0.15-0.5 Hz) frequency ranges. Cerebral autoregulation was assessed from the transfer function gain and phase shift between LF oscillations of blood pressure and cerebral blood flow velocity. In the diabetic patients, lower body negative pressure decreased the RR-interval, i.e. increased heart rate, while blood pressure and cerebral blood flow velocity decreased. Transfer function gain and phase shift remained stable. Lower body negative pressure did not induce the normal increase in sympathetically mediated LF-powers of blood pressure and cerebral blood flow velocity in our patients indicating sympathetic dysfunction. The stable phase shift, however, suggests intact cerebral autoregulation. The dying back pathology in diabetic neuropathy may explain an earlier and greater impairment of peripheral vasomotor than cerebrovascular control, thus maintaining cerebral blood flow constant and protecting patients from symptoms of presyncope.

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