Pathophysiology Of Postural Tachycardia Syndrome Research Articles

Etiologies and Management of Postural Tachycardia Syndrome in Children

Postural tachycardia syndrome (POTS) is a chronic condition with frequent symptoms of orthostatic intolerance or with sympathetic activation and excessive tachycardia while standing, without significant hypotension. The aim of this review was to discuss the pathogenesis and to outline the diagnosis and treatment guidelines. We conducted a literature review of articles published up to 2017, in following databases; PubMed, and Embase investigating postural tachycardia syndrome in children. We restricted our search to only English published articles with human subjects concerning children under 16 years. POTS is a disorder of the autonomic nervous system that could create considerable disability amongst previously healthy people. Patients with POTS show a HR rise of ≥ 30 bpm within 10 min of standing (or greater in kids), are typically hyperadrenergic, and tend to have a reduced blood volume. The pathophysiology of POTS is complex and the result of a variety of separate systems producing a common pattern of signs. The specific pathogenesis of POTS has yet not been completely clear. A variety of uncommon factors might be involved in the pathogenesis. Selecting the correct therapy according to the detailed pathogenesis could absolutely enhance the efficiency of medicine. Treatments targeting the hypovolemia and the excess sympathetic nervous system activation may assist eliminate symptoms.

Renin-Aldosterone Paradox and Perturbed Blood Volume Regulation Underlying Postural Tachycardia Syndrome

Patients with postural tachycardia syndrome (POTS) experience considerable disability, but in most, the pathophysiology remains obscure. Plasma volume disturbances have been implicated in some patients. We prospectively tested the hypothesis that patients with POTS are hypovolemic compared with healthy controls and explored the role of plasma renin activity and aldosterone in the regulation of plasma volume. Patients with POTS (n=15) and healthy controls (n=14) underwent investigation. Heart rate (HR), blood pressure (BP), plasma renin activity, and aldosterone were measured with patients both supine and upright. Blood volumes were measured with 131I-labeled albumin and hematocrit. Patients with POTS had a higher orthostatic increase in HR than controls (51+/-18 versus 16+/-10 bpm, P<0.001). Patients with POTS had a greater deficit in plasma volume (334+/-187 versus 10+/-250 mL, P<0.001), red blood cell volume (356+/-128 versus 218+/-140 mL, P=0.010), and total blood volume (689+/-270 versus 228+/-353 mL, P<0.001) than controls. Despite the lower plasma volume in patients with POTS, there was not a compensatory increase in plasma renin activity (0.79+/-0.58 versus 0.79+/-0.74 ng x mL(-1) x h(-1), P=0.996). There was a paradoxically low level of aldosterone in the patients with POTS (190+/-140 pmol/L versus 380+/-230 pmol/L; P=0.017). Patients with POTS have paradoxically unchanged plasma renin activity and low aldosterone given their marked reduction in plasma volume. These patients also have a significant red blood cell volume deficit, which is regulated by the renal hormone erythropoietin. These abnormalities suggest that the kidney may play a key role in the pathophysiology of POTS.

Clinical and Laboratory Indices That Enhance the Diagnosis of Postural Tachycardia Syndrome

To identify clinical and laboratory indices that improve the diagnosis of the postural tachycardia syndrome (POTS). We assessed associations of orthostatic intolerance by using multivariate regression analysis. We evaluated autonomic symptoms and autonomic function in 30 patients with POTS, 30 patients with mild orthostatic intolerance, and 19 age- and gender-matched control subjects. Indices of parasympathetic and sympathetic functions were analyzed on the basis of (1) autonomic function tests (head-up tilt), (2) oscillations at respiratory and nonrespiratory frequencies (0.01 to 0.09 Hz) in R-R interval and blood pressure (Wigner distribution), and (3) deterministic component (rescaled range analysis). The four clinical and laboratory indices that independently supported the diagnosis of POTS are as follows: (1) orthostatic heart rate during the first minute of head-up tilt, (2) autonomic deficit (adrenergic autonomic score), (3) loss of spectral powers in R-R interval during head-up tilt at the fifth minute, and (4) severity of orthostatic dizziness, fatigue, palpitations, and shortness of breath. Enhancing the sensitivity and specificity of the diagnosis of POTS should be possible by using these four indices. A hyperadrenergic state and distal neuropathy, affecting adrenergic sympathetic cardiovagal fibers, seem to be involved in the pathophysiology of POTS. Certain features suggest brain-stem dysregulation.