title: Potassium removal increases the QTc interval dispersion during hemodialysis.
abstract: This study was planned to clarify the mechanism(s) by which hemodialysis increases the QTc dispersion, a marker of risk of ventricular arrhythmias. To this aim, 10 uremic patients, without any relevant heart diseases, underwent two different types of hemodialysis schedules. In the first, 1 h of isolated high rate ultrafiltration preceded the standard diffusive procedure. In the second, during the first hour of standard bicarbonate hemodialysis, the decrease of plasma potassium concentration was prevented by increasing K+ concentration in the dialysate, according to its pre dialysis plasma levels. During the high rate ultrafiltration period, together with ECG signs of increased sympathetic nervous system activity and catecholamines secretion, the QTc dispersion did not change significantly. Instead, an evident increment was observed 1 h after the start of the diffusive hemodialysis, then slowly progressing until the end of the dialysis and finally returning to the pre dialysis values within 2 h after the end of the session. To the contrary, the increase of the QTc dispersion was totally blunted during a standard hemodialysis procedure in absence of plasma K+ decrease, but appeared again when the K+ dialysate fluid concentration was restored to 2 mmol/l. This study provides evidence that the increase of QTc dispersion occurring on hemodialysis is mainly related to the diffusive process, more precisely to the K+ removal. This is one more reason to focus attention on K+ removal rate especially when hemodialysis treatment is given in uremics affected by cardiac diseases with high risk of arrhythmias.
authors.affiliation: Dipartimento di Medicina Interna, Università di Pisa, Pisa, Italia.
authors.forename: A
authors.initials: A
authors.lastname: Cupisti
authors.forename: F
authors.initials: F
authors.lastname: Galetta
authors.forename: R
authors.initials: R
authors.lastname: Caprioli
authors.forename: E
authors.initials: E
authors.lastname: Morelli
authors.forename: G C
authors.initials: GC
authors.lastname: Tintori
authors.forename: F
authors.initials: F
authors.lastname: Franzoni
authors.forename: A
authors.initials: A
authors.lastname: Lippi
authors.forename: M
authors.initials: M
authors.lastname: Meola
authors.forename: P
authors.initials: P
authors.lastname: Rindi
authors.forename: G
authors.initials: G
authors.lastname: Barsotti
mesh_terms: D001794:Blood Pressure / Q000502:physiology; D002395:Catecholamines / Q000097:blood; D003404:Creatinine / Q000378:metabolism; D004562:Electrocardiography; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000502:physiology*; D011191:Potassium Deficiency / Q000378:metabolism; D006435:Renal Dialysis / Q000009:adverse effects*; D014508:Urea / Q000378:metabolism; D014883:Water-Electrolyte Imbalance / Q000209:etiology / Q000378:metabolism
chemical_list: D002395:Catecholamines; D014508:Urea; D003404:Creatinine; D011188:Potassium