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      Haemodynamic consequences of changing potassium concentrations in haemodialysis fluids

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          Abstract

          Background

          A rapid decrease of serum potassium concentrations during haemodialysis produces a significant increase in blood pressure parameters at the end of the session, even if effects on intra-dialysis pressure are not seen. Paradoxically, in animal models potassium is a vasodilator and decreases myocardial contractility. The purpose of this trial is to study the precise haemodynamic consequences induced by acute changes in potassium concentration during haemodialysis.

          Methods

          In 24 patients, 288 dialysis sessions, using a randomised single blind crossover design, we compared six dialysate sequences with different potassium profiles. The dialysis sessions were divided into 3 tertiles, casually modulating potassium concentration in the dialysate between the value normally used K and the two cut-off points K+1 and K-1 mmol/l. Haemodynamics were evaluated in a non-invasive manner using a finger beat-to-beat monitor.

          Results

          Comparing K-1 and K+1, differences were found within the tertiles regarding systolic (+5.3, +6.6, +2.3 mmHg, p < 0.05, < 0.05, ns) and mean blood pressure (+4.3, +6.4, -0.5 mmHg, p < 0.01, < 0.01, ns), as well as peripheral resistance (+212, +253, -4 dyne.sec.cm -5, p < 0.05, < 0.05, ns). The stroke volume showed a non-statistically-significant inverse trend (-3.1, -5.2, -0.2 ml). 18 hypotension episodes were recorded during the course of the study. 72% with K-1, 11% with K and 17% with K+1 (p < 0.01 for comparison K-1 vs. K and K-1 vs. K+1).

          Conclusions

          A rapid decrease in the concentration of serum potassium during the initial stage of the dialysis-obtained by reducing the concentration of potassium in the dialysate-translated into a decrease of systolic and mean blood pressure mediated by a decrease in peripheral resistance. The risk of intra-dialysis hypotension inversely correlates to the potassium concentration in the dialysate.

          Trial Registration Number

          NCT01224314

          Related collections

          Most cited references 27

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          Effects of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical trials.

           P K Whelton,  J. He,  J Cutler (1997)
          To assess the effects of supplementation with oral potassium on blood pressure in humans. Meta-analysis of randomized controlled trials. English-language articles published before July 1995. Thirty-three randomized controlled trials (2609 participants) in which potassium supplementation was the only difference between the intervention and control conditions. Using a standardized protocol, 2 of us independently abstracted information on sample size, duration, study design, potassium dose, participant characteristics, and treatment results. By means of a random-effects model, findings from individual trials were pooled, after results for each trial were weighted by the inverse of its variance. An extreme effect of potassium in lowering blood pressure was noted in 1 trial. After exclusion of this trial, potassium supplementation was associated with a significant reduction in mean (95% confidence interval) systolic and diastolic blood pressure of -3.11 mm Hg (-1.91 to -4.31 mm Hg) and -1.97 mm Hg (-0.52 to -3.42 mm Hg), respectively. Effects of treatment appeared to be enhanced in studies in which participants were concurrently exposed to a high intake of sodium. Our results support the premise that low potassium intake may play an important role in the genesis of high blood pressure. Increased potassium intake should be considered as a recommendation for prevention and treatment of hypertension, especially in those who are unable to reduce their intake of sodium.
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            Role of potassium in regulating blood flow and blood pressure.

            Unlike sodium, potassium is vasoactive; for example, when infused into the arterial supply of a vascular bed, blood flow increases. The vasodilation results from hyperpolarization of the vascular smooth muscle cell subsequent to potassium stimulation by the ion of the electrogenic Na+-K+ pump and/or activating the inwardly rectifying Kir channels. In the case of skeletal muscle and brain, the increased flow sustains the augmented metabolic needs of the tissues. Potassium ions are also released by the endothelial cells in response to neurohumoral mediators and physical forces (such as shear stress) and contribute to the endothelium-dependent relaxations, being a component of endothelium-derived hyperpolarization factor-mediated responses. Dietary supplementation of potassium can lower blood pressure in normal and some hypertensive patients. Again, in contrast to NaCl restriction, the response to potassium supplementation is slow to appear, taking approximately 4 wk. Such supplementation reduces the need for antihypertensive medication. "Salt-sensitive" hypertension responds particularly well, perhaps, in part, because supplementation with potassium increases the urinary excretion of sodium chloride. Potassium supplementation may even reduce organ system complications (e.g., stroke).
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              A systematic review of the clinical effects of reducing dialysate fluid temperature.

              Intradialytic hypotension (IDH) is a frequent complication of haemodialysis. Reducing the temperature of the dialysis fluid is a simple therapeutic strategy but is relatively underused. This may be due to concerns regarding its effects on symptoms and dialysis adequacy. We performed a systematic review of the literature to examine the effects of cool dialysis on intradialytic blood pressure, and to assess its safety in terms of thermal symptoms and small solute clearance. We searched the Cochrane Central Register of Controlled Trials, Medline, Embase, Cumulative Index to Nursing and Allied Health Literature, databases of ongoing trials, the contents of four major renal journals as well as hand-searching reference lists. We included all prospective randomized studies that compared any technique of reducing dialysate temperature with standard bicarbonate dialysis. These techniques included an empirical, fixed reduction of dialysate temperature or use of a biofeedback temperature-control device (BTM) to deliver isothermic dialysis or programmed patient cooling. A total of 22 studies comprising 408 patients were included (16 studies examined a fixed empirical temperature reduction and six examined BTM). All studies were of crossover design and relatively short duration. IDH occurred 7.1 (95% CI, 5.3-8.9) times less frequently with cool dialysis (both fixed reduction and BTM). Post-dialysis mean arterial pressure was higher with cool-temperature dialysis by 11.3 mmHg (95% CI, 7.7-15.0). No studies reported that cool dialysis led to a reduction in dialysis adequacy as assessed by urea clearance. The frequency and severity of thermal-related symptoms were generally reported inadequately. Reducing the temperature of the dialysate is an effective intervention to reduce the frequency of IDH and does not adversely affect dialysis adequacy. This applies to the fixed reduction of dialysate temperature and BTM. It remains unclear as to what extent cool-temperature dialysis causes intolerable cold symptoms during dialysis. There are no trials comparing fixed empirical temperature reduction with BTM, and no trials examining the long-term effects of cool dialysis on patient outcomes.
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                Author and article information

                Journal
                BMC Nephrol
                BMC Nephrology
                BioMed Central
                1471-2369
                2011
                6 April 2011
                : 12
                : 14
                Affiliations
                [1 ]Division of Nephrology, Ospedale la Carità, Via Ospedale, 6600 Locarno, Switzerland
                [2 ]Department of Internal Medicine, Ospedale la Carità, Locarno, Switzerland
                [3 ]Division of Nephrology, University Hospital of Lausanne, Lausanne, Switzerland
                Article
                1471-2369-12-14
                10.1186/1471-2369-12-14
                3079606
                21470404
                Copyright ©2011 Gabutti et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Research Article

                Nephrology

                hypotension, potassium, dialysis fluids, haemodynamics, haemodialysis

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