Venous Dysfunction and the Change of Blood Viscosity During Head‐Up Tilt

Abstract

The precise stimulus that induces vasovagal syncope is still unclear. We have previously demonstrated that the peripheral distribution of blood volume (venous pooling) is a strong predictor of tilt induced vasovagal reaction. We hypothesized that an increase in venous pooling during tilt accentuates the measured increase in blood viscosity. This hypothesis is based on the previously demonstrated increase in venous pressure and subsequent increase in transcapillary fluid transudation during tilt. The increased blood viscosity, in turn, increases vascular shear rate, which may alter the vasoconstrictive and other cardiovascular responses to decreased preload. We measured blood viscosity (supine and tilt) in 56 patients with a history of orthostatic intolerance (37 with venous pooling [VP] and 19 without venous pooling [non-VP]). VP and non-VP were separated into subgroups based on blood pressure and heart rate response to tilt. There was a positive correlation between blood viscosity and plasma aldosterone in the supine. In the group as a whole, neither supine blood viscosity nor its increase during tilt differed between VP and non-VP. However, the tilt induced increase of blood viscosity was significant only in patients with tilt provoked tachycardia plus normal blood pressure response in VP group. We suggest that the increase of blood viscosity in this group led to the normal blood pressure response. The positive correlation between supine blood viscosity and supine plasma aldosterone indicates that the normal blood pressure response in this group possibly was via stimulation of the renin-angiotensin-aldosterone system.

Postural Tachycardia Syndrome and Reflex Syncope: Similarities and Differences

“…41,42 Contributions may also arise from changes in hematocrit and in blood viscosity. 43 Of these variants the redistributive form is most common. This has been attributed to lower extremity blood pooling and vasodilation in “neurogenic POTS,” 44,45 or to our category of “normal flow POTS” in which splanchnic vasodilation and blood pooling occur.…”

Haemodynamic response to peripheral venous congestion in patients with unexplained recurrent syncope

“…The decrease in venous return to the heart by an exaggerated shift in blood volume from central to peripheral vascular bed has been suspected as a precipitating factor for the development of syncope [3,4]. A trend for greater peripheral blood pooling and a reduced venous volume variability was reported in patients with neurally mediated syncope [5], whereas another study failed to clearly demonstrate the relationships between venous pooling, blood viscosity and head-up tilt (HUT) [6]. Other studies have suggested impaired change in peripheral venous tone [5,7], although no differences in venous compliance between controls and patients with postural tachycardia syndrome have been reported [8].…”

“…Interpretation and the predictive value of these findings remains limited by the small number of subjects studied with various etiologies for syncope (e.g. orthostatic intolerance [6] and postural tachycardia [8]), leaving the contribution of both exaggerated venous pooling and impaired circulatory adjustment to be clarified in the routine diagnostic framework of syncope of unexplained origin. In our present study, the heterogeneity of etiologies for syncope was reduced by the exclusion of patients with postural tachycardia.…”

Active compression garment prevents tilt‐induced orthostatic tachycardia in humans

“…This blood redistribution results in a decrease in blood return to the heart, subsequently causing a decrease in stroke volume, cardiac output, and ultimately blood pressure (Yamanouchi et al. ; Dorey et al. ).…”