Volume Status and Blood Pressure During Long-Term Hemodialysis

Abstract

Abstract-The importance of volume status on blood pressure in hemodialysis patients has long been recognized. We hypothesized that the enhanced volume dependency of blood pressure is partly determined by ventricular stiffness at end systole. A total of 115 long-term hemodialysis patients were invited to receive a comprehensive, noninvasive cardiovascular examination. End-systolic elastance was determined by using a novel, noninvasive echo-Doppler technique. The positive ratios of the interdialytic systolic blood pressure change vs weight gain during the subsequent 25 hemodialysis sessions were averaged to obtain the volume sensitivity index (mm Hg/kg). H ypertension is present in Ϸ80% to 90% of patients by the time chronic renal failure progresses to end-stage renal disease (ESRD) and is one of the major risk factors that contributes to the development of cardiovascular disease in patients undergoing dialysis. 1,2 A rational approach to this issue necessitates insight into the mechanisms that underlie hypertension in renal failure. 1 Volume expansion has long been considered the most important factor in the development and maintenance of hypertension in ESRD. 1,2 It is well accepted that hypertension can be controlled by adequate dialysis and the maintenance of dry weight in 85% to 90% of dialysis patients. In one center in Tassin, France, almost 98% of the patients were normotensive while receiving no medication by long, slow dialysis. 3,4 In contrast, Ϸ50% of hypertensive patients without renal function impairment are considered salt-sensitive and respond to diuretic therapy alone. 5,6 Thus, it is obvious that the sensitivity of blood pressure change to volume expansion or removal in patients with ESRD is increased compared with hypertensive patients with normal renal function. The mechanisms by which volume expansion leads to an elevation in blood pressure are conventionally attributed to an increase in cardiac output and an inappropriately high systemic vascular resistance. 1 We have demonstrated that arterial stiffening with age is matched by ventricular systolic stiffening, indexed by the end-systolic pressure-volume relation (ie, left ventricular end-systolic elastance, E es ). 7 The two effects contribute to elevating systolic blood pressure (SBP) sensitivity to acutely altered chamber filling 7 and might explain the enhanced pressure lability with diuretics and postural shifts in the elderly. Although E es implies the sensitivity of SBP to acute volume reduction, it is unknown whether E es also predicts changes in SBP with long-term volume change. On the other hand, increased arterial stiffness as a hemodynamic overload with consequential and parallel cardiac and vascular adapta-

Brachial-ankle vs carotid-femoral pulse wave velocity as a determinant of cardiovascular structure and function

“…24 Arterial load and stiffness were also indexed by the effective arterial elastance (Ea), which is equal to the ratio of LV end-systolic pressure divided by stroke volume (SV). 6 LV end-systolic pressure was estimated from brachial systolic blood pressure  0.9, 9 and SV was measured by pulse-wave Doppler echocardiography. 9 Augmentation index was analysed from the right common carotid artery pressure wave contour using the method described previously.…”

“…6 LV end-systolic pressure was estimated from brachial systolic blood pressure  0.9, 9 and SV was measured by pulse-wave Doppler echocardiography. 9 Augmentation index was analysed from the right common carotid artery pressure wave contour using the method described previously. 17,25 Augmentation index was the ratio of the augmented pressure, which was determined as the height of the late systolic peak above the inflection point, to the pulse pressure in percentage.…”

“…5 The combined ventricular arterial stiffening has clinical implications in the decreased exercise tolerance in the elderly, 6,7 heart failure with preserved ejection fraction 8 and enhanced volume sensitivity of blood pressure in haemodialysis patients. 9 Furthermore, arterial stiffening contributes to the process of atherosclerosis and arterial disease by influencing the shear stress imposed on the blood vessel walls and endothelial function. 5 In fact, the stiffness over the central arteries assessed by measuring pulse wave velocity (PWV) between the carotid and femoral arteries (carotid-femoral pulse wave velocity, cf-PWV) has been validated as an independent, strong marker for future cardiovascular events in patients with hypertension, 2 diabetes 3 and renal failure, 4 and in the general population 10 and apparently healthy subjects.…”

Dietary salt intake of Bangladeshi patients with kidney disease in East London: An exploratory case study

“…1 Hypertension is both cause and consequence of CKD 2 and extracellular volume expansion is an important factor in the development and maintenance of hypertension in CKD patients. 3 The British Bangladeshi population has an unusually high salt intake, twice that of the general population, which might contribute to both CKD and hypertension. 4 Patients with resistant hypertension, defined as BP that remains above target despite the use of three or more antihypertensive medications 5 , are thought to be salt sensitive.…”

Acute vs chronic volume overload on arterial stiffness in haemodialysis patients

“…12 The presence of heart failure may also increase the sensitivity of volume change on stroke volume, cardiac output, and arterial mechanical property. Furthermore, the frequently seen calcific degeneration of the mitral annulus and aortic valve may influence the interpretations of vascular parameters.…”