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 accumulation of uremic toxins and their rapid removal with dialysis causing 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 QTc interval.
Method:
6 anuric HD patients were enrolled in a 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 minutes were assessed during a 4 hour HFR Supra dialysis session, the subsequent 7 hours and at the start of the following session after 48 hours. A 12 lead ECG were 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-hours after dialysis. Dialysate electrolytes were: Na 140 mEq/L, K 3 mEq/L, Ca2+ 1.5 mEq/L, 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, 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 are resumed the in vivo results of the 5 patients regarding Ke, Ki, Ki/Ke, Ca2+ and QTc during and after HFR. In Figure 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, while 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 to 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+
