Dialysis Prescription and Sudden Death

Abstract

In the United States, end-stage renal disease patients receiving hemodialysis have an exceedingly high risk of sudden cardiac death (SCD), accounting for 29% of death events, likely relating to their uremic milieu, recurring exposure to fluid and electrolyte fluxes, and underlying cardiovascular pathology. Furthermore, epidemiologic studies have shown that SCD events, as well as mortality and hospitalizations, occur most frequently on the first dialysis day following the long interdialytic gap, suggesting that abrupt fluctuations in the accumulation and removal of electrolytes, fluid, and uremic toxins over the dialysis cycle may be contributory. Some population based observational studies have suggested that lower dialysate potassium concentrations appear associated with heightened risk of post-dialysis cardiac arrest in hemodialysis patients, although the optimal serum-to-dialysate potassium gradient remains unclear. Some observational studies suggests that low dialysate calcium concentrations and high serum-to-dialysate calcium gradients may predispose to SCD. There is ongoing controversy about an association betweenhigher dialysate bicarbonate concentrations and higher risk of cardiac arrest, which is likely due to confounding by indication. Some observational studies have also shown that large interdialytic weight gains, fluid retention, and high ultrafiltration (UFR) rates are linked with higher risk of SCD and mortality. However, there remains considerable controversy regarding the pros and cons of designating a specific upper UFR limit with extended treatment times as a clinical practice measure, and further studies are needed to define the optimal tools, metrics, targets, and implementation measures for volume control in the hemodialysis population. In this Review, we highlight the epidemiology and pathophysiology of how specific aspects of the hemodialysis procedure may relate to the risk of SCD, as well as preventative strategies and future research directions that can address this risk.

A simple modification of dialysate potassium: its impact on plasma potassium concentrations and the electrocardiogram

“…Several authors have suggested that such hypokalaemia induced by dialysis could trigger arrhythmias, and especially ventricular arrhythmias [ 5 , 21 ]. The excess occurrence of arrhythmia and sudden death in the first hours after the dialysis are session has been described and would be consistent with the role for post-dialysis hypokalaemia [ 4–7 , 13–15 , 17 , 34 , 35 ]. In addition, there may be a higher risk of mortality and sudden death in dialysis patients treated with low dialysate K [ 4 , 8 , 9 , 12–15 , 17 , 18 , 25 , 28–30 , 36 , 37 ].…”

“…Abnormalities of potassium (K) before and after dialysis session, and rapid changes in K concentrations during the dialysis session have been suggested as a potential cause of arrhythmia [ 5 , 7 , 12 , 13 , 20–22 ]. Hyperkalaemia before dialysis session is frequent, dangerous and increases morbidity and mortality [ 7 , 17 , 18 , 22–30 ]. Additional data also suggest that pre-dialysis hypokalaemia, although less frequent, could be associated with higher mortality [ 11 , 13 , 22 , 25 , 27 , 30–32 ].…”

Variations in Magnesium Concentration Are Associated with Increased Mortality: Study in an Unselected Population of Hospitalized Patients

“…Here, we showed that variations in magnesium concentration are associated with in-hospital mortality. This is in line with the observations of Rhee et al, who showed that fluctuations in magnesium concentration in dialyzed patients constitute a risk factor for increased mortality [ 39 ]. In our study, the highest variations in magnesium concentration were associated with hematological malignancies, septic shock, and multi-organ disfunction.…”

“…To conclude, it has been shown that disturbances in magnesium homeostasis accompany systemic diseases and severe conditions [ 39 , 40 , 43 ]. Either hypo- or hyper-magnesemia are associated with increased risk of mortality, and, for this reason, primarily, hypermagnesemia should be treated as a laboratory biomarker of critical value.…”

Dialysis-Induced Cardiovascular and Multiorgan Morbidity

“…8,18,64,106,108 In addition, the combined effects of cardiocirculatory stress, hypovolemia, and electrolyte changes may create proarrhythmogenic conditions. 99,[123][124][125] Cardiac changes as a result of myocardial stunning, cardiac remodeling in response to cyclical pressure and volume overload, fibrotic scarring, and loss of contractile function with aberrant electrical conductivity are all pathways that conceivably increase the sudden cardiac death risk. 59,98,99,[126][127][128] These findings have similarities with the extreme physiologic demands that are experienced by healthy subjects under adverse environmental conditions, with the difference that they must be endured repeatedly by a vulnerable patient population over months and years.…”