Higher Dialysate Sodium Research Articles

Fluid-Shift during Computer-Modulated Profile Hemodialysis (Cmp-Hd)

Computer-modulated profile hemodialysis was examined for patients' comfort and fluid-shift. Fifteen patients were studied after two weeks of dialysis with each of the following profiles: A): constant ultrafiltration (UF) and dialysate sodium (138 mmol/l); B): decreasing UF; C): decreasing UF and decreasing high dialysate sodium (starting 10% above serum-sodium, with a gradual reduction to 138 mmol/l in the fourth hour). Patients with a calculated increase of intracellular volume (ICV) during dialysis had more complaints after dialysis than the others. ICV decreased in all patients with low serum-sodium (less than 136 mmol/l) during all profiles, whereas in patients with higher sodium, only profile C led to a decrease of ICV. However, interdialytic weight gain increased about 75% in patients with low serum-sodium under profile C. The sodium profile could help in preventing imbalance without side effects in patients with high sodium.

Influence of High and Low Sodium Dialysis on Blood Volume Preservation

Haemodialysis has a profound effect on fluid balance. Since fluid is initially withdrawn from the intravascular compartment, hypovolaemia is a frequent complication. A fluid shift from the overhydrated interstitium towards the intravascular compartment can counteract hypovolaemia. However, a fast decline in extracellular osmolality may cause an increase in the intracellular volume, reducing the available amount of fluid to compensate for the hypovolaemia. To overcome this problem, the use of alternating high and low sodium dialysate is advocated. In this study six patients were studied during standard haemodialysis (HD) and during dialysis with alternating high and low sodium dialysate (HLSD). Changes in intracellular fluid volume (IFV) and extracellular fluid volume (EFV) of tissue and blood were measured by means of a non-invasive electrical conductivity method. Changes in blood volume (BV) were studied by serial erythrocyte counts. Plasma sodium concentration was determined at regular intervals. The distribution volume of sodium during the high and low sodium episodes of HLSD was calculated according to a mathematical model. HLSD led to fluctations in plasma sodium concentration that induced changes in red cell volume, but not in IFV. Distribution of sodium was largely confined to blood. BV was better preserved during HLSD than during HD, probably due to a higher mean plasma sodium concentration. Postdialysis sodium concentration however, was not significantly different between HLSD and HD. These data suggest that the better BV preservation during HLSD results from an induced osmotic gradient across the capillary wall, rather than from an osmotic gradient across the cell membrane.

Fluid Balance During Haemodialysis and Haemofiltration: The Effect of Dialysate Sodium and a Variable Ultrafiltration Rate

One of the main causes of hypotension during extracorporeal renal replacement therapy is an insufficient substitution of the ultrafiltrated plasma water by tissue water. To investigate the fluid balance and its effects on hypotension in dialysed patients, the following variables were studied: intracellular fluid volume (IFV) and extracellular fluid volume (EFV), blood volume (BV) and blood pressure. IFV and EFV were measured by means of non-invasive electrical conductivity measurements using four electrodes round the leg. Fifteen haemofiltration (HF) and 15 haemodialysis (HD) patients were studied. The latter group was dialysed in three ways: (1) conventionally, i.e. with dialysate sodium of 138 mmol/l (HD) (2) with a variable dialysate sodium (first half: 138 mmol/l; second half: 146 mmol/l) (HDS), and (3) with the same variable dialysate sodium and an ultrafiltration profile (two-thirds was withdrawn during the first half of treatment, the remainder during the second half) (HDSU). Hypotension frequency was less during HDS, HDSU, and HF compared to HD. This was caused by a more stable blood volume due to a better refill. During HD a fluid shift occurred from the EC to the IC compartment. The use of a high sodium dialysate concentration led to a transcellular fluid shift in the opposite direction. This fluid shift increased the refill, thereby stabilising blood volume. HF gave a better refill than HDS and HDSU, probably due to a reduced urea clearance.

Interstitial Correction of Blood Volume Decrease during Hemodialysis

The etiology of hypotension during hemodialysis is multifactorial. Probably a decrease in blood volume caused by ultrafiltration, and acetate are both involved, while refilling from the interstitium acts as a compensatory mechanism. An osmotically induced transcellular fluid shift to intracellular might reduce the refilling capacity. This study investigated the effect of ultrafiltration on blood volume, blood pressure and refilling. The role of acetate and blood volume decrease in hypotension was established and intra- and extracellular fluid changes were calculated. Blood volume decrease depended on ultrafiltration: at high ultrafiltration rates refilling failed, apparently more so at high acetate plasma levels. An isolated blood volume decrease did not lower blood pressure. Concomitant high acetate levels caused hypotension and also seemed to reduce refilling. Nearly all refilling fluid came from the extracellular compartment. Only high dialysate sodium concentrations gave rise to an intracellular loss.

Acetate dialysate versus bicarbonate dialysate: a continuing controversy.

The use of bicarbonate dialysate as the buffer during routine dialysis is growing. This discussion reviews several of the comparative trials in which bicarbonate and acetate buffers have been tested. Effects of the two buffers on BP, cardiac function, and pulmonary performance are discussed. Costs of the two systems are also compared. Patients who seem most likely to benefit from bicarbonate dialysate include those with a reduced muscle mass in whom a high sodium dialysate has not prevented hypotension.

Effects of high sodium dialysate during maintenance hemodialysis.

The effects of high sodium 144 mmol/l (mEq/l) dialysate were studied in normotensive, hypertensive and anephric chronic hemodialysis patients. Comparisons of blood pressures, weights and side effects associated with the hemodialysis procedure were made between two 6-month periods using dialysate sodium concentration of 133 mmol/l (mEq/l), followed by a high dialysate sodium of 144 mmol/l (mEq/l), each patient acting as his own control. No difference was found in the frequency of cramps or 'disequilibrium' side effects (nausea, vomiting, headache, restlessness). High sodium dialysate is beneficial for normotensive and anephric patients in reducing dialysis-induced hypotension and was not associated with any deleterious effects on long-term blood pressure control. In hypertensive patients, the benefit is less clear, and hypertension may increase.

Acetate and bicarbonate hemodialysis in patients with and without autonomic dysfunction

To test the contribution of bicarbonate (Bi) to hemodynamic stability during hemodialysis (HD), we compared the effects of ultrafiltration dialysis with bicarbonate and with acetate under conditions of high-sodium (141 mEq/liter) and low-sodium (130 mEq/liter) dialysate concentrations in 12 stable HD patients. Group 1 was patients (N = 5) who had normal findings on autonomic testing; group 2, patients (N = 7) who had abnormal findings on autonomic testing. All patients and staff were unaware of which dialysis was being used. During the high-sodium dialysate studies, changes in mean blood pressure (MBP), cardiac output (CO), and orthostatic tolerance to standing after HD were similar in both groups of patients with both acetate and bicarbonate dialysate. When the studies were repeated under low-sodium dialysate conditions, several differences emerged between acetate and bicarbonate HD. In group 1, the frequency of adverse symptoms upon standing after HD were reduced with bicarbonate (P less than 0.05). In group 2, bicarbonate HD prevented a significant decrease in orthostatic MBP after HD. These results suggest that bicarbonate affords no greater hemodynamic stability than does acetate if a dialysate sodium of 141 mEq/liter is used. With lower sodium dialysate, bicarbonate appears to provide a modest improvement in decreasing orthostatic symptoms and signs in patients with and without autonomic insufficiency.

High sodium bicarbonate and acetate hemodialysis: Double-blind crossover comparison of hemodynamic and ventilatory effects

The superiority of bicarbonate dialysis (Bi HD) over acetate dialysis (Ac HD) using a high sodium dialysate has not been established to our knowledge. We compared to Bi HD to Ac HD over 6 weeks each in ten stable patients using a double-blind crossover design and a dialysate sodium concentration of 140 mEq/liter. The dialyzer, delivery system, and disalysate constituents were identical except for the substitution of Bi or Ac. Interdialytic weight gain, pre- and post-HD blood pressures, and heart rates were also comparable in the two protocols. Beginning of the week pre-HD serum Bi was greater during Bi HD than Ac HD (19.1 +/- 0.9 vs. 15.1 +/- 0.8 mEq/liter, P less than 0.001); post-HD Bi values were also higher during Bi HD. Similarly, pre-HD pH was also greater with Bi HD 7.40 +/- 0.012 vs. 7.35 +/- 0.001 U, P less than 0.01). The number of adverse symptoms and signs were similar during each protocol (2.0 +/- 0.65 for Bi HD vs. 2.5 +/- 0.5 for Ac HD episodes/patient/6 weeks, NS). However, fewer therapeutic interventions were required during the Bi HD protocol (1.5 +/- 0.43 vs. 3.1 +/- 0.6 treatments/patient/6 weeks, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical features of high sodium dialysate and hemofiltration.

Clinical features of high sodium dialysate and hemofiltration.

Effect of dialysate sodium concentration on the appearance of ischemic EKG patterns.

This study was undertaken to evaluate the effect of increasing the dialysate sodium concentration on myocardial ischemia assessed by EKGs taken immediately before and after dialysis in 43 hemodialysis patients. An increase in the R wave (V5 + V6) by more than 5 mm was seen in 26 patients with standard sodium dialysate, while only 12 cases showed the same changes after a high sodium dialysis. These was a positive correlation between an increase in R wave amplitude and the weight loss/dry weight ratio of patients only after standard sodium dialysis (r = 0.74, p less than 0.001). Relative high sodium dialysate is beneficial during dialysis and reduce the incidence of myocardial ischemia and unpleasant disequilibrium syndrome.

The role of acetate in the etiology of symptomatic hypotension.

Acetate, although widely used as the source of buffer in hemodialysis, has been implicated in the development of symptomatic hypotension and hypoxemia during dialysis. Studies of acetate infusion clearly indicate a vasodilatory effect. Acetate also increases cardiac output. If the increase in cardiac output is not adequate to compensate for the decrease in peripheral resistance, hypotension can result. Acetate infusion studies indicate a significant increase in oxygen consumption. This may be the most plausible explanation for dialysis-induced hypoxemia. Correction of the hypoxemia with supplemental oxygen has been shown to reduce the incidence of hypotensive episodes and intradialytic symptoms. Studies comparing cardiovascular stability during acetate and bicarbonate dialysis indicate that bicarbonate dialysis is beneficial only when the fall in serum osmolality during dialysis is significant. If the fall in serum osmolality is blunted either with a high-sodium dialysate or mannitol infusions, there is little difference between acetate and bicarbonate. From a practical viewpoint, high-sodium dialysis is technically less complex and expensive than bicarbonate dialysis.

Controversy in renal disease: dialysis-induced hypotension.

HEMODIALYSIS is remarkably safe. Death due to technical failure or humanerror occurs in only about 1 in 75,000 treatments. The resilience of the cardiovascular system can be appreciated from its ability to tolerate hours of extracorporeal blood circulation at flow rates of 300 mVmin or greater. Very few patients develop true shock during or as an immediate consequence of hemodialysis. A substantial proportion, however, become hypotensive to the extent that postdialysis malaise limits prompt return to predialysis physical activities in many otherwise well rehabilitated patients. Little attention was devoted to the understanding of dialysis-induced hypotension in the first decade of maintenance hemodialysis perhaps, because patient and physician viewed this complication as an unavoidable side effect of a wondrous new therapy. Subsequently, lessons learned in the mid 1970s, from clinical trials of postdilutional hemofiltration, and reexploration of the utility of bicarbonate (rather than acetate) buffering of dialysate, now suggest that dialysis-induced hypotension may be minimized or prevented under certain conditions. Keshaviah and Shapiro examine eight variables (their Table 1) which could account for a fall in blood pressure during or after dialysis and state that its genesis is . . complex, controversial, and multifactorial. With laudable caution, Keshaviah and Shapiro decline to indict a single causative mechanism though they conclude that at low dialysate sodium concentrations acetate . . is associated with a more marked fall of blood pressure than is bicarbonate. Heneghan accepts the evidence tying acetate to hypotension and explores the question of Why is acetate associated with greater morbidity during dialysis? In a simple but telling double-blind experiment, Heneghan administered oxygen or compressed air to five patients during 30 hemodialyses to test his thesis that acetate-caused hypoxemia was responsible for hypotension. In this study, when hypoxemia was prevented by oxygen, hypotension was avoided and dialysis was better tolerated. According to Heneghan, acetate metabolism reduces CO2 production which in turn induces hypoventilation and hypoxemia. Recognizing that long term comparisons of acetate and bicarbonate have not been done, Heneghan nevertheless concludes that . . acetate must be considered suspect. Directors of dialysis units must weigh the data for themselves to determme whether or not to invest in machines equipped to infuse bicarbonate as the principal dialysate buffer. In my view, the case is still open. Adding another pump increases the probability of mechanical error. Until the controlled studies called for by both essayists are performed, nearly all patients prone to hypotension can be managed by using a normal or high dialysate sodium concentration combined with administration of nasal oxygen throughout dialysis.

A critical examination of dialysis-induced hypotension.

Dialysis-induced hypotension has received considerable attention recently because of its high incidence of occurrence. Several factors have been proposed as etiologic mechanisms. They include hypovolemia, autonomic dysfunction, decreasing serum osmolality, vasodilation (or the inhibition of compensatory vasoconstriction), efficiency of diffusive solute transport, depletion of vasoactive substances and blood gas and acid-base changes. The primary determinants of blood pressure being cardiac output and total peripheral resistance, the magnitude and direction of change of these two parameters determines the blood pressure response. If the rate of ultrafiltration exceeds the rate of vascular refilling, hypovolemia results. Intracellular fluid shifts secondary to preferential solute removal from the extracellular space may compromise vascular refilling and contribute to hypovolemia. If the hypovolemia is not compensated for by increases in heart rate or stroke volume, the cardiac output falls. Autonomic dysfunction, a previous history of myocardial infarction or impaired tissue oxygenation secondary to hypoxia may limit compensatory increases in heart rate and stroke volume. Even if the cardiac output falls, if compensatory vasoconstriction is elicited, blood pressure can be maintained. The experimental evidence suggests that the diffusive aspect of dialysis therapy plays an important role in inhibiting compensatory vasoconstriction. Such inhibition is not observed with hemofiltration, a therapy based on convective rather than diffusive solute removal. While autonomic dysfunction and the diffusive removal of vasoactive substances may play a role in inhibiting the vasoconstrictive response, the use of acetate as a buffer source and the decreasing serum osmolality seem to be of greater importance. Acetate produces vasodilation. It also has a positive inotropic effect. Studies suggest that the vasodilation produced by acetate is compensated for by a proportionate increase in cardiac output except during the early stages of the therapy when the fall in total peripheral resistance may overwhelm the increase in cardiac output. The substitution of bicarbonate for acetate results in a decrease in the incidence of symptomatic hypotension in some patients. This alleviation of symptoms appears to be significant only when the dialystate sodium concentration is relatively low (130–135 m M ). At higher dialysate sodium concentrations (140–145 m M ), the blunting of the fall in serum osmolality seems to be of greater importance than the nature of the buffer source in reducing the incidence of symptomatic hypotension. It is not clear if blunting the fall in serum osmolality has a greater beneficial influence on the cardiac output or on the total peripheral resistance. While the etiology of dialysis-induced hypotension is complex, controversial, and multifactorial, amelioration of symptomatic hypotension with a higher dialysate sodium concentration offers a practical solution. The substitution of bicarbonate for acetate is a technically more complex and expensive alternative.

Reduction of Calcium Transfer to Body with High Sodium Dialysate

Reduction of Calcium Transfer to Body with High Sodium Dialysate

Programmed infusion system for high sodium dialysate

Programmed infusion system for high sodium dialysate