Hemodialysis with acetate, DL-lactate and bicarbonate: A hemodynamic and gasometric study

Abstract

Using invasive techniques we have studied various hemodynamic and gasometric parameters in the course of hemodialysis (HD) with different buffers in an animal model. HD sessions of 180 minutes at zero ultrafiltration were carried out on three groups of eight uremic dogs each, under anesthesia and constant mechanical ventilation. The three groups differed only in the buffer used: acetate (Group AC), equal proportions of DL-lactate and acetate (Group AC+LA), and bicarbonate (Group BC). No hemodynamic changes were seen in Group BC. In the AC and AC+LA groups we observed on minute 1 a decrease of the mean blood pressure (MBP) and of the systemic vascular resistances (SVR). These parameters returned to baseline values within the first 30 minutes in Group AC+LA. In Group AC the SVR also returned to baseline values after the minute 30, but the MBP remained below baseline throughout the study period, together with cardiac index and left ventricular stroke work index decreases. Only in Group AC did we see a flattening of the ventricular function curves. Only in this Group was there a decrease of the arterial oxygen pressure (PaO2) with an associated increase of the alveolo-arterial and arterio-venous O2 differences. The O2 consumption was not modified in any of the groups. Acetate as a single buffer induces hemodynamic instability through peripheral vasodilation and reduction of myocardial contractility. The myocardial depression induced by acetate, in its turn, causes a reduction in PaO2. The mixed acetate+lactate buffer is hemodynamically better tolerated than acetate as single buffer, as it induces only vasodilation.

Effects of Acetate-Free Double-Chamber Hemodiafiltration and Standard Dialysis on Systemic Hemodynamics and Troponin T Levels

“…It remains contentious as to whether acetate transfer during dialysis causes myocardial depression. Although several studies do show that acetate causes a reduction in myocardial contractility, [3][4][5][6] there are other studies that do not confirm this. It has been postulated that acetate directly affects myocardial contractility, although it is also possible that increased endothelial NO production stimulated by acetate affects the baroreflex arc.…”

“…Acetate has been shown to cause vasodilatation that is mediated by nitric oxide release, but has also been shown to reduce myocardial contractility. [3][4][5][6] Many of these studies were carried out in animal models, and debate remains about validity of the results from some of the studies in humans.…”

Model-based study of the effects of the hemodialysis technique on the compensatory response to hypovolemia

“…Among these factors, the composition and quality of dialysate, filter membrane biocompatibility, and the convection/diffusion rate seem to influence the patient's tendency to acute hypotension. As a pertinent example, the replacement of most of the acetate with bicarbonate in standard hemodialysis has resulted in a decrease in intradialytic hypotensive episodes [10][11][12]. The role of acetate has been attributed to an acetate-induced impairment of cardiovascular reactivity.…”

Sodium Acetate as a Replacement for Sodium Bicarbonate in Medical Toxicology: a Review

“…Sodium acetate, when given in excess during dialysis, is funneled to alternative metabolic pathways, leading to increased nitric oxide concentrations and resulting hemodynamic instability [25]. Several animal studies have reported decreased systemic vascular resistance (SVR) in response to sodium acetate [26][27][28]. Research into the association of pooled protein fraction infusion and hypotension implicated sodium acetate, at concentrations as low as 16.8 mEq/L, as the cause of hypotension [26].…”

“…This has not been reproduced in other studies. Sodium acetate dialysate buffer, when compared head-to-head with sodium bicarbonate dialysate, consistently lowers SVR [27,28]. Hypopnea, often in the setting of hypoxemia during dialysis with sodium acetate, may arise from loss of carbon dioxide in the absence of a bicarbonate buffer; chemoreceptors then recognize serum hypocarbia and reduce respiratory drive [22].…”