MO749: QTC Interval, Potassium and Electrolytes Kinetics During and after Dialysis with Supra HFR (Pandora Study)

Abstract

Abstract BACKGROUND AND AIMS The QTc interval is a marker of arrhythmic risk in dialysis patients, and its lengthening has been associated with an increased risk of sudden death [1]. This phenomenon could be due to the accumulation of uremic toxins and their rapid removal with dialysis causing an imbalance of electrolytes currents [2]. The aim of the study is to describe the kinetics of potassium (K+) and other electrolytes during and after dialysis with the goal of validate a mathematical model for predicting the respective kinetics [3]. The secondary endpoint is to identify a correlation between the kinetics of intra (Ki) and extracellular K+ (Ke) during and after dialysis and the QTc interval. METHOD A total of 6 anuric HD patients were enrolled in an interventional, exploratory, prospective study. Clinical and pharmacological factors favouring the onset of arrhythmias or influencing the total mass of K + were excluded. Ki and Ke, Ca2+ Na, blood gas analysis, glucose and urea every 30 min were assessed during a 4 h HFR Supra dialysis session, the subsequent 7 h and at the start of the following session after 48 h. A 12-lead ECG was performed with the same schedule, and a bioimpedance vector analysis (BIVA) was obtained at the start and the end of the dialysis and 1 and 7 h after dialysis. Dialysate electrolytes were Na 140 mEq/L, K 3 mEq/L, Ca2+ 1.5 mEq/L and HCO3– 30 mmol/L. A selective ion probe was used to measure K+; the Ki value was obtained by an indirect formula expressed in a previous study [4]. The model of K + kinetics includes the Na+/K+/ATPase-dependent pump, the passive diffusion of K + from the intracellular to the extracellular compartment, the diffusion of K + through the filter, the intradialytic volume variation, the K + and solute rebound after dialysis, and the role of plasma osmolality [3]. RESULTS The model showed a better correlation to the in vivo data during the HFR phase than the post-dialytic one regarding Ke, sodium, HCO3– and Ca2+. The wide variability recorded by Ki is significantly in contrast with the stability predicted by the model, and the entity of post-dialysis Ca2+ drop was greater than that predicted by the model. Kinetics prediction of urea had a precise fitting with in vivo data in every phase. In Table 1, the in vivo results of the 6 patients regarding Ke, Ki, Ki/Ke, Ca2+ and QTc during and after HFR are resumed. In Fig. 1, we see the data extrapolated from a patient (likewise the others), where the greatest waving of the QTc occurred in the first hour post HFR in parallel with fluctuations of Ki and Ki/Ke. CONCLUSION The mathematical model for the prediction of the kinetics of solutes has shown a good correspondence with the in vivo data of K+, sodium, urea, Ca2+ and HCO3– during HFR, although it still needs to be refined in the post-dialysis phase. The major discrepancies for Ki could be due to difficult analytical processing. As to the greater drop of Ca2+ compared with the predicted, it can be due to the role played by other Ca2+ compartments in addition to the intra and extracellular ones. Although during the intradialytic period we faced a shortening of the QTc interval with a significant reduction in Ke, greater Ki/Ke and an increase in Ca2+ the post-HFR period appeared to be the most critical period. This phase corresponded to the largest fluctuations in QTc values, Ki, Ki/Ke ratio, and to the rapid rebound of K + and the drop of Ca2+.