Orthostatic hypotension is a sustained and pathological drop in blood pressure upon standing. Orthostatic hypotension can be due to non-neurogenic conditions or autonomic
disorders. Impaired baroreflex-mediated vasoconstriction and insufficient release of norepinephrine play key roles in the pathophysiology of neurogenic orthostatic hypotension. Its common symptoms mainly related to inadequate cerebral blood flow include dizziness, lightheadedness, and syncope. It is crucial to differentiate neurogenic orthostatic hypotension from non-neurogenic orthostatic hypotension. For the management of neurogenic orthostatic hypotension, physicians should implement non-pharmacological methods and, if possible, reverse combined non-neurological conditions. Depending on severity of symptoms, pharmacological intervention may be tried after or with non-pharmacological methods. Its management should be individualized based on intensity of symptoms, comorbid conditions, drug side effects, and etiology. In this review, we discuss the definition, pathophysiology, clinical approach, and management of neurogenic orthostatic hypotension.
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Orthostatic dizziness is feeling dizzy or lightheaded when standing up. Hemodynamic orthostatic dizziness can be caused by autonomic dysfunction such as orthostatic hypotension or postural tachycardia syndrome. The interpretation of the autonomic function test results in patients with orthostatic dizziness is crucial for diagnosing and managing the underlying condition. The head-up tilt and Valsalva tests are especially important for evaluating adrenergic function in patients with hemodynamic orthostatic dizziness. However, it is important to note that autonomic function tests do not cover the entire diagnostic process, since their findings need to be considered along with the detailed history and physical examination results of the patient because various differential diagnoses exist for orthostatic dizziness. Ensuring appropriate treatment by interpreting the autonomic function test results can help to determine the improvement of and prevents falls from orthostatic dizziness.
We present a patient with a primitive neuroectodermal tumor arising from the right atrium who experienced multiple syncope episodes daily, which had first appeared 1 month after surgery. The symptoms continued to worsen over the course of chemotherapy, and the autonomic function test (AFT) was performed after the 14th chemotherapy cycle. The AFT revealed orthostatic hypotension and reduced baroreflex-dependent sympathetic reactivity. Physical counterpressure techniques were applied with a visual biofeedback intervention, and were found to be effective in reducing the syncope episodes.
This paper introduces new diagnostic criteria and differential diagnosis of orthostatic dizziness to help clinicians to diagnose hemodynamic orthostatic dizziness. Clinicians need to be able to discriminate hemodynamic orthostatic dizziness from other types of dizziness that are induced or aggravated when standing or walking. Measurements of the orthostatic blood pressure and heart rate are important when screening hemodynamic orthostatic dizziness. Detailed history-taking, a physical examination, and laboratory tests are essential for finding the cause of hemodynamic orthostatic dizziness. The differential diagnosis of hemodynamic orthostatic dizziness is crucial because it can be caused by various autonomic neuropathies.
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Mareo y vértigo ortostático, funcional y cinetosis Liliana F. Invencio-Da-Costa, Carmen Sánchez-Blanco, Raquel Yáñez-González, Hortensia Sánchez-Gómez, Paula Peña-Navarro, Sofía Pacheco-López, Susana Marcos-Alonso, Cristina Nicole Almeida-Ayerve, Luis Cabrera-Pérez, Victoria Díaz-Sánchez Revista ORL.2023; 15(3): e31540. CrossRef
Background Orthostatic hypotension (OH) refers to a fall in systolic blood pressure (BP) of 20 mmHg or more, or indiastolic BP of 10 mm Hg or more within 3 minutes of standing up. The head-up tilt test (HUT) is the most useful, butpotentially invasive test for the diagnosis of OH. The purpose of this study was to identify the usefulness of spontaneousbaroreflex sensitivity (sBRS). Methods: Ninety one patients with orthostatic intolerance, in whom the HUT data were available,were included in the study. Patients were classified into HUT-positive (group I) and HUT-negative (group II) group.Twenty five healthy volunteers served as normal controls, and were designated as group III. In all subjects, beat-to-beat BPand heart rate were recorded using BeatScope 1.1a. We collected the 50 sBRS data in each patient in a supine position.The average value of one to ten of 50 sBRS data was defined as sBRS10, one to twenty as sBRS20, one to thirty as sBRS30, one to forty as sBRS 40, and one to fifty as sBRS 50. Differences in sBRS10 and sBRS50 levels were statisticallyanalyzed and compared between groups I, II, and III. Results: No significant difference in the sBRS50 level was found betweenGroups II and III. sBRS50 was significantly lower in Group I than in Groups II and III (p<0.05), and the same patternof differences was observed for sBRS40, sBRS30, sBRS20, and sBRS10. Conclusions: Patients with OH showed significantlylower sBRS levels than HUT-negative patients or normal controls. Our study implies that a supine-position sBRS would provideadditional diagnostic information for OH.