Changes In Serum Potassium Concentration Research Articles

Lethal ventricular arrhythmia can be prevented by adjusting the dialysate potassium concentration and the use of anti-arrhythmic agents: a case report and literature review

BackgroundHypokalemia is common in patients with malnutrition undergoing hemodialysis and is often involved in the development of lethal arrhythmia. Moreover, hemodialysis therapy decreases the serum potassium concentration due to potassium removal to the dialysate. However, it is difficult to adjust the dialysate potassium concentration owing to the use of the central dialysate delivery system in Japan. Here, we have presented a case undergoing hemodialysis with dialysate potassium concentration adjustment to prevent ventricular arrhythmia.Case presentationA 56-year-old man with Emery-Dreifuss muscular dystrophy and chronic heart failure was admitted to our hospital and needed subsequent hemodialysis therapy due to renal dysfunction. During hemodialysis, the cardiac resynchronization therapy defibrillator was activated to the treatment of his lethal ventricular arrhythmia. Decreases in serum potassium concentration after hemodialysis and changes in serum potassium concentration during HD were considered the causes of lethal ventricular arrythmia. Therefore, along with using anti-arrhythmic agents, the dialysate potassium concentration was increased from 2.0 to 3.5 mEq/L to minimize changes in the serum potassium concentration during hemodialysis. Post-dialysis hypokalemia disappeared and these changes during hemodialysis were minimized, and no lethal ventricular arrhythmia occurred thereafter.ConclusionsIn this case, we prevented lethal arrhythmia by maintaining the serum potassium concentration by increasing the dialysate potassium concentration, in addition to the use of anti-arrhythmic agents. In the acute phase of patients with frequent lethal arrhythmia undergoing hemodialysis, an increase in dialysate potassium concentration may be an effective method for preventing arrhythmogenic complications.

MO364: Population Pharmacodynamic Dose-Response Analysis of Serum Potassium Following Dosing With Sodium Zirconium Cyclosilicate

Abstract BACKGROUND AND AIMS Sodium zirconium cyclosilicate (SZC, LOKELMA®) is an orally administered suspension for treating hyperkalemia that permits selective, monovalent cation exchange and has a high exchange capacity for potassium cations in the gut leading to a net reduction in systemic potassium. The goals of the analysis were to describe the population pharmacodynamic response of serum potassium concentration (S-K) in hyperkalemic subjects treated with SZC; specifically, the longitudinal dose response of SZC for S-K in correction (0–48 h) and maintenance (>48 h) phases of treatment, and the differences in S-K response among populations identified by their intrinsic and extrinsic factors. METHOD A population pharmacodynamic model was developed using serum potassium, dose timing/amount, and patient demographic and medical history data pooled from 7 phase 2 and 3 clinical studies consisting of 2369 subjects with hyperkalemia (screening S K >5 mmol/L) with a total of 25 764 S-K observations. A virtual pharmacokinetic-pharmacodynamic model (K-PD) model was used to mimic a drug exposure without any measurements (none were available, drug was not absorbed). S-K over time was described by an indirect response model where potassium enters/leaves a compartment corresponding to serum potassium measurements. The impact of SZC exposure was modeled as an inhibition of the potassium production rate, consistent with the SZC mechanism of action to bind potassium and lower its absorption and appearance in circulation. RESULTS Diagnostics indicated good agreement between the observed data and the model, for mean S-K and change from baseline, and overall qualified the model as appropriate for predicting S-K changes following SZC dosing. The sigmoid exposure response on Kin was characterized by a high value for the EC50 (32.8 g) and a hill coefficient of 1.36. Not surprisingly, within the range of doses studied (0–15 g), the dose response appeared nearly linear. The placebo adjusted S-K change from baseline for QD maintenance treatment was 0.37 (95% CI –0.42 to –0.32) for 5 g, –0.75 (95% CI –0.82 to –0.65) for 10 g, and –1.06 (95% CI –1.17 to –0.89) for 15 g. Greater treatment response was associated with high S-K at baseline, more advanced age, lower body weight and lower eGFR. Furthermore, greater treatment response was also predicted for Black or African American and Asian patients, compared with Caucasian individuals, but they remained unworthy of dose adjustment. Lastly, dose-response simulations show no clinically meaningful difference between maintenance regimens of 5 g QOD and 2.5 g QD in the studied patient groups. CONCLUSION The population K-PD model of SZC adequately described the changes in serum potassium concentration during correction and maintenance phase dosing in the seven clinical studies. Greater treatment response was associated with high S-K at baseline, more advanced age, lower body weight, lower eGFR, Black or African American race and Asian race; however, the impact of each covariate was modest. The overall results of this analysis support the conclusion that no dose adjustment is needed for SZC based on any of the tested covariates.

Safety of a Nurse-Driven Standardized Potassium Replacement Protocol in Critically Ill Patients With Renal Insufficiency.

In critically ill patients, maintaining appropriate serum potassium concentrations requires careful supplementation to correct hypokalemia but avoid hyperkalemia. At the study institution, an institution-based, nurse-driven standardized electrolyte replacement protocol is used in critically ill patients with a serum creatinine concentration of 2 mg/dL or less. If the serum creatinine concentration is greater than 2 mg/dL, electrolyte replacement requires a physician order. To determine if standardized potassium supplementation is safe in critically ill patients with renal insufficiency not requiring renal replacement therapy. This study was an institutional review board-approved, single-center, retrospective evaluation of critically ill patients receiving intravenous potassium replacement per protocol. Patients were grouped according to serum creatinine concentration (≤ 2 mg/dL or > 2 mg/dL) at the time of replacement. The primary outcome was the incidence of hyperkalemia (potassium concentration ≥ 5 mEq/L) following potassium replacement. Secondary outcomes were the incidence of hyperkalemia, change in serum potassium concentration, and need for hyperkalemia treatment. Outcomes were analyzed using χ2 and t tests. Of 814 patients screened, 145 were included (99 with serum creatinine ≤ 2 mg/dL and 46 with serum creatinine > 2 mg/dL). The incidence of hyperkalemia was not different between groups (P = .57). Five patients experienced hyperkalemia; none received hyperkalemia treatment. Change in serum potassium was similar for patients in the 2 groups (P = .33). A standardized, nurse-driven electrolyte replacement protocol can be used safely in critically ill patients with renal insufficiency not requiring renal replacement therapy.

Extracorporeal potassium binding for the management of hyperkalemia in an anephric model of crush injury.

Potassium-binding polymers have shown promising results in an anephric porcine hyperkalemia model. The benefits of the polymer in a clinically relevant injury model remain unknown. We hypothesized that potassium-binding cartridges would control serum potassium concentration in a porcine hemorrhagic shock model with supraceliac aortic occlusion and a limb crush injury. Ten Yorkshire-cross swine were anesthetized and instrumented. Pigs underwent splenectomy and bilateral nephrectomy. Hemorrhagic shock was induced for 30 minutes while a leg compression device was applied. Pigs underwent supraceliac aortic occlusion for 60 minutes and were resuscitated with shed blood. The leg compression device was removed 20 minutes after balloon deflation. After 20 minutes of reperfusion, animals were randomized to extracorporeal circulation with (treatment) or without (control) the potassium binding cartridges. In both groups, blood was circulated through a hemodialyzer with a peristaltic pump. In the treatment group, the ultrafiltrate was diverted from the hemodialyzer through cartridges containing the polymer and returned to the extracorporeal circuit. Animals were resuscitated with 0.9% saline boluses and a norepinephrine infusion. The change in serum potassium concentration (ΔK) was calculated as serum [K]T390 - serum [K]T0. There was a significant difference in serum potassium concentration between groups (p < 0.001). ΔK was significantly higher in the control than the treatment group (3.75 [3.27-4.42] and 1.15 [0.62-1.59] mmol/L, respectively; p = 0.03). There were no differences in mean arterial pressure (p = 0.14), isotonic crystalloids requirement (p = 0.51), or norepinephrine dose (p = 0.83) between groups. Serum lactate concentration was significantly higher in the control group (p < 0.001). At the end of the experiment, the [K] was reduced by 25% (24.9%-27.8%) across the cartridges. The cartridges controlled serum potassium concentrations without dialysate and retained potassium binding capabilities over 4 hours. There were no deleterious effects on hemodynamic parameters. Those cartridges might be beneficial adjuncts for hyperkalemia management in austere environments. Translational science study, level I.

Dialysate and Serum Potassium in Hemodialysis

Most patients with end-stage renal disease depend on intermittent hemodialysis to maintain levels of serum potassium and other electrolytes within a normal range. However, one of the challenges has been the safety of using a low-potassium dialysate to achieve that goal, given the concern about the effects that rapid and/or large changes in serum potassium concentrations may have on cardiac electrophysiology and arrhythmia. Additionally, in this patient population, there is a high prevalence of structural cardiac changes and ischemic heart disease, making them even more susceptible to acute arrhythmogenic triggers. This concern is highlighted by the knowledge that about two-thirds of all cardiac deaths in dialysis are due to sudden cardiac death and that sudden cardiac death accounts for 25% of the overall death for end-stage renal disease. Developing new approaches and practice standards for potassium removal during dialysis, as well as understanding other modifiable triggers of sudden cardiac death, such as other electrolyte components of the dialysate (magnesium and calcium), rapid ultrafiltration rates, and safety of a number of medications (ie, drugs that prolong the QT interval or use of digoxin), are critical in order to decrease the unacceptably high cardiac mortality experienced by hemodialysis-dependent patients.

Rationale and design of ARTS: a randomized, double‐blind study of BAY 94‐8862 in patients with chronic heart failure and mild or moderate chronic kidney disease

BAY 94-8862 is a novel, non-steroidal, mineralocorticoid receptor antagonist with greater selectivity than spironolactone and stronger mineralocorticoid receptor binding affinity than eplerenone. The aims of the MinerAlocorticoid Receptor Antagonist Tolerability Study (ARTS; NCT01345656) are to evaluate the safety and tolerability of BAY 94-8862 in patients with heart failure associated with a reduced left ventricular ejection fraction (HFREF) and chronic kidney disease (CKD), and to examine the effects on biomarkers of cardiac and renal function. Methods ARTS is a multicentre, randomized, double-blind, placebo-controlled, parallel-group study divided into two parts. In part A, oral BAY 94-8862 [2.5, 5, or 10 mg once daily (o.d.)] is compared with placebo in ∼60 patients with HFREF and mild CKD. Outcome measures include serum potassium concentration, biomarkers of renal injury, estimated glomerular filtration rate (eGFR), and albuminuria. Part B compares BAY 94-8862 (2.5, 5, or 10 mg o.d., or 5 mg twice daily), placebo, and open-label spironolactone (25-50 mg o.d.) in ∼360 patients with HFREF and moderate CKD. Outcome measures include the change in serum potassium concentration with BAY 94-8862 vs. placebo (primary endpoint) and vs. spironolactone, safety and tolerability, biomarkers of cardiac and renal function or injury, eGFR, and albuminuria. BAY 94-8862 pharmacokinetics are also assessed. Perspectives ARTS is the first phase II clinical trial of BAY 94-8862 and is expected to provide a wealth of information on BAY 94-8862 in patients with HFREF and CKD, including the optimal dose range for further studies.

Risk of hyperkalemia associated with selective COX-2 inhibitors

Selective cyclooxygenase-2 (COX-2) inhibitors have been linked to cardiac death. The mechanism for this adverse effect appears to be by ischemic insult; however another mechanism could involve hyperkalemia. The objective of this study was to determine the effects of selective COX-2 inhibitors and non-selective nonsteroidal anti-inflammatory drugs (NSAIDs) on serum potassium concentration and the electrocardiogram. A retrospective cohort study was conducted using propensity score matching of patients from an inner-city academic medical center at Indianapolis, Indiana. Two hundred and two patients prescribed selective COX-2 inhibitors were matched to 202 patients prescribed non-selective NSAIDs using propensity scores methods. Outcomes included change in serum potassium concentration from baseline and the risk of an abnormal electrocardiogram. Compared to patients prescribed non-selective NSAIDs, those prescribed a selective COX-2 inhibitor had a higher risk of serum potassium increase greater than 5 mEq/L (OR, 2.56; 95%CI, 1.03-6.36). However, patients prescribed selective COX-2 inhibitors had no greater risk of electrocardiogram abnormality (OR, 1.16; 95%CI, 0.74-1.82). Selective COX-2 inhibitors may have a greater risk of hyperkalemia than non-selective NSAIDs. This study was exploratory with small numbers of patients. Further studies are needed to confirm these results and any association with cardiovascular events.

A Randomized Controlled Trial of Fludrocortisone for the Treatment of Hyperkalemia in Hemodialysis Patients

Previous small uncontrolled studies suggested that fludrocortisone may significantly decrease serum potassium concentrations in hemodialysis patients, possibly through enhancement of colonic potassium secretion. The aim of this study is to evaluate the effect of oral fludrocortisone on serum potassium concentrations in hyperkalemic hemodialysis patients in an open-label randomized controlled trial. Thirty-seven hemodialysis patients with predialysis hyperkalemia were randomly allocated to administration of either oral fludrocortisone (0.1 mg/d; n = 18) or no treatment (control; n = 19) for 3 months. The primary outcome measure was midweek predialysis serum potassium concentration, which was measured monthly during the trial. Prospective power calculations indicated that the study had an 80% probability of detecting a decrease in serum potassium levels of 0.7 mEq/L (0.7 mmol/L). Baseline patient characteristics were similar, except for slightly longer total weekly dialysis hours in the fludrocortisone group (13.0 +/- 1.3 versus 12.1 +/- 1.0; P = 0.02). At the end of the study period, no significant changes in serum potassium concentrations were observed between the fludrocortisone and control groups (4.8 +/- 0.5 versus 5.2 +/- 0.7 mEq/L [mmol/L], respectively; P = 0.10). Similar results were obtained when changes in serum potassium levels over time were examined between the 2 arms by using repeated-measures analysis of variance, with or without adjustment for total weekly dialysis hours. Secondary outcomes, including predialysis mean arterial pressure, interdialytic weight gain, serum sodium level, and hospitalization for hyperkalemia, were not significantly different between groups. There were no observed adverse events. Administering fludrocortisone to hyperkalemic hemodialysis patients is safe and well tolerated, but does not achieve clinically important decreases in serum potassium levels.

Potassium intake during cell dehydration

Isotonic NaCl is ingested in addition to water by cell-dehydrated rats in two-bottle tests. The objective of the present work was to find out whether mineral intake in the cell-dehydrated rat is specific to NaCl in a five-bottle test. Adult male Sprague Dawley rats had distilled water and four mineral solutions at palatable concentrations (0.01 M KCl, 0.05 mM CaCl 2, 0.15 M NaHCO 3, 0.15 M NaCl) simultaneously available for consumption. Cell-dehydration was produced infusing 1.5 ml of NaCl solution (0.15, 0.25, 0.5, 1.0, 2.0, 4.0 M) intravenously for 10 min and intakes were recorded for the next hour. It was observed a NaCl concentration-dependent increase in 0.01 M KCl intake. The ingestion of the other mineral solutions was not significantly altered compared to infusion of 0.15 M NaCl. The ingestion of KCl was not related to changes in serum potassium concentration. The ingestion of KCl was reduced in half and water was the preferred fluid when the five-bottle test was performed with mineral solutions at isomolar (0.15 M) concentrations. There was no increase in intake of other mineral solution in the isomolar test. No preference was observed for palatable or isomolar solutions during early extracellular dehydration until 4 h after subcutaneous injection of furosemide, in spite of the increase in total volume intake. Therefore, mineral intake induced by cell dehydration is not specific for NaCl solution. The type of mineral solution available influences the choice and KCl is the preferred solution of the cell-dehydrated rat in the conditions of the present study.

Serum Potassium and Acid-base Parameters in Severe Dialysis-associated Hyperglycemia Treated with Insulin Therapy

We analyzed the changes in serum potassium concentration ([K]) and acid-base parameters in 43 episodes of dialysis-associated hyperglycemia (serum glucose level > 33.3 mmol/L), 22 of which were characterized as diabetic ketoacidosis (DKA) and the remaining 21 as nonketotic hyperglycemia (NKH). All episodes were treated with insulin therapy only. Age, gender, initial and final serum values of glucose, sodium, chloride, tonicity and osmolality did not differ between DKA and NKH. At presentation, serum values of [K] (DKA 6.2 +/- 1.3 mmol/L; NKH 5.2 +/- 1.5 mmol/L) and anion gap [AG] (DKA 27.2 +/- 6.4 mEq/L; NKH 15.4 +/- 3.5 mEq/L) were higher in DKA, whereas serum total carbon dioxide content [TCO2 ] (DKA 12.0 +/- 4.6 mmol/L; NKH 22.5 +/- 3.1 mmol/L), arterial blood pH (DKA 7.15 +/- 0.09; NKH 7.43 +/- 0.07) and arterial blood PaCO2 (DKA 26.2 +/- 12.3 mm Hg; NKH 34.5 +/- 6.7 mm Hg) were higher in NKH. At the end of insulin treatment, serum values of [K] (DKA 4.0 +/- 0.7 mmol/L, NKH 4.0 +/- 0.5 mmol/L), [AG] (DKA 16.3 +/- 5.4 mEq/L, NKH 14.9 +/- 3.0 mEq/L), [TCO2 ] (DKA 23.5 +/- 5.0 mmol/L, NKH 24.1 +/- 4.2 mmol/L), arterial blood pH (DKA 7.42 +/- 0.09, NKH 7.51 +/- 0.14) and arterial blood PaCO2 (DKA 31.8 +/- 6.7 mm Hg, NKH 34.2 +/- 8.3 mm Hg) did not differ between the two groups. Linear regression of the decrease in serum [K] value during treatment, (Delta[K]), on the presenting serum [K] concentration,([K]2 ), was: DKA, Delta[K] = 2.78 - 0.81 x [K]2 , r = -0.85, p < 0.001; NKH, Delta[K] = 2.44 - 0.71 x [K]2 , r = -0.90, p < 0.001. The slopes of the regressions were not significantly different. Stepwise logistic regression including both DKA and NKH cases identified the presenting serum [K] level and the change in serum [TCO2 ] value during treatment as the predictors of Delta[K] (R2 = 0.81). Hyperkalemia is a feature of severe hyperglycemia (DKA or NKH) occurring in patients on dialysis. Insulin administration brings about correction of DKA and return of serum [K] concentration to the normal range in the majority of the hyperglycemic episodes without the need for other measures. The initial serum [K] value and the change in serum [TCO2 ] level during treatment influence the decrease in serum [K] value during treatment of dialysis-associated hyperglycemia with insulin.

Response of the QT interval to mental and physical stress in types LQT1 and LQT2 of the long QT syndrome

OBJECTIVETo study and compare the effects of mental and physical stress on long QT syndrome (LQTS) patients.DESIGNCase–control study.MAIN OUTCOME MEASURESQT intervals were measured from lead V3. Serum potassium and plasma catecholamine concentrations were also monitored.PATIENTS16 patients with type 1 LQTS (LQT1), 14 with type 2 LQTS (LQT2), both groups asymptomatic, and 14 healthy control subjects.INTERVENTIONSThree types of mental stress tests and a submaximal exercise stress test.RESULTSHeart rate responses to mental stress and exercise were similar in all groups. During mental stress, the mean QT interval shortened to a similar extent in controls (–29 ms), LQT1 patients (–34 ms), and LQT2 patients (–30 ms). During exercise, the corresponding QT adaptation to exercise stress was more pronounced (p &lt; 0.01) in healthy controls (–47 ms) than in LQT1 (–38 ms) or LQT2 patients (–38 ms). During exercise changes in serum potassium concentrations were correlated to changes in QT intervals in controls, but not in LQTS patients. LQT1 and LQT2 patients did not differ in serum potassium, catecholamine or heart rate responses to mental or physical stress.CONCLUSIONSQT adaptation to mental and exercise stress in healthy people and in patients with LQTS is different. In healthy people QT adaptation is more sensitive to physical than to mental stress while no such diverging pattern was seen in asymptomatic LQTS patients.

Heparin-Mediated Hypotension Associated with Cardiac Surgery

To the Editor: We read with great interest the article by Jacka and Clark (1) describing an association among heparin administration, hyperkalemia, and hypotension/bradycardia during cardiac surgery. We recently observed a similarly severe hypotensive episode in a cardiac surgical patient in response to heparin administration; however, absence of hyperkalemia in our case necessitates an alternative pathophysiologic explanation. The patient, a 58-yr-old man with unstable angina and an otherwise unremarkable medical history, was admitted for coronary artery bypass graft surgery. Preoperative medications included ranitidine and metoprolol. After an uneventful anesthetic induction with midazolam and fentanyl and surgical isolation of the internal mammary artery, administration of 300 U/kg of porcine heparin through the central venous catheter resulted, within 90 s, in a 35% reduction in arterial blood pressure (123/59 to 80/40 mm Hg). Heart rate remained unchanged at 70 bpm. Intraoperative transesophageal echocardiography revealed no abnormalities in left ventricular function, and no acute changes in the electrocardiogram were noted. Administration of phenylephrine in two 100-μg doses corrected the arterial pressure. Laboratory findings before the hypotensive episode and 10 min after were unremarkable with no change in serum potassium concentration (K = 4.3 mmol/L). Several reports have described an association between hypotension and heparin administration preceding cardiopulmonary bypass (1–3). In a prospective investigation, Urban et al. (3) reported hypotension in 17 of 20 patients in response to 300 U/kg heparin. Although generally less dramatic than the hypotension observed in our case, a 13% decrease in arterial pressure occurred within 76 ± 26 s of heparin administration. The authors further demonstrated a correlation between serum ionized calcium concentrations and the hypotensive response. Administration of small doses of calcium chloride before heparin administration increased serum ionized calcium concentration and abolished the hypotensive response. In a subsequent prospective investigation, Casthely et al. (4) demonstrated an association between heparin-mediated hypotension and histamine release. H1-receptor blockade significantly attenuated the hypotensive response to heparin; in contrast, patients receiving only H2-receptor blockade experienced an exaggerated hypotensive response. Although a hyperkalemic response to heparin, as described by Jacka and Clark (1), may be associated with hemodynamic instability, it is unlikely to be the primary cause. Instead, vasodilation secondary to heparin-mediated hypocalcemia and/or histamine release appear more likely mechanisms. Clinically significant episodes of heparin-mediated hypotension are uncommon. However, in those few cases of prolonged and/or exaggerated hypotension, administration of calcium chloride or a specific vasoconstrictor is reasonable. In patients with a history of a clinically significant hypotensive response to heparin, preoperative administration of an H1-receptor blocker may be prudent. Thomas F. Slaughter MD Jonathan B. Mark MD

Hypokalemia and agitation in acute psychotic patients

Hypokalemia is caused partly by intensive exercise. Some evidence suggests that psychological distress may cause hypokalemia. The relationship between the decline of serum potassium concentration and the level of symptoms of acute agitation, which was defined as a total score on a subset of six categories on the 18-item Brief Psychiatric Rating Scale (anxiety, tension, mannerism and posturing, hostility, uncooperativeness, psychomotor excitement), was examined in 313 schizophrenic men, admitted on an emergency basis during a 24-month period. In addition, change in serum potassium concentration after sedation was investigated. Serum potassium concentration in the severely agitated group was lower than that in the mild group. There was a significant correlation between serum potassium concentration and the level of symptoms of acute agitation ( r=−0.30, P<0.0001). Although the decline of serum potassium concentration in the patients who were sufficiently sedated improved within 8 h, that in the patients showing high scores on the acute agitation subset even 8 h after emergency admission was prolonged. Results indicate that sedation improves acute agitation-induced hypokalemia.

The Effect of Magnesium Pretreatment on Serum Potassium Concentration and Hemodynamic State in Rabbits during Continuous Regular Insulin(RI) Infusion

Background : Insulin is known to act as second effector that provides potassium transfer from extracellular fluid to intracellular fluid, thus causing hypokalemia and arrythmia. We evaluated the effect of magnesium sulfate treatment on hemodynamics and serum potassium concentration, induced by continuous infusion of regular insulin solution in rabbits. Method : Twenty-four rabbits were divided into four groups for the experiment. Group I was given intravenouse injection of 5 ml of normal saline and continuous dripping of 7.5 U of RI. Group II was pretreated with 30 mg/kg of magnesium sulfate, followed by continuous dripping of 7.5 U of RI. Group III was given 5 ml of normal saline and 15 U of RI. And Group IV was administered 15 U of RI after 30 mg/kg of magnesium sulfate pretreatment. Venouse blood sampling was done before pretreatment, and after 5, 30, 60 and 120 minutes respectively. Heart rate and arterial blood pressure were taken at the same intervals. Result : 1) There was no significant change in serum potassium concentration in groups injected with 7.5 units of RI respectively (groups I and II), regardless of magnesium pretreatment. But in groups injected with 15 units of RI, the group that was not pretreated with magnesium (Groups III) showed a decrease in serum potassium concentration from 3.39 0.57 Eq/L to 2.29 0.71 mEq/L, while the concentration in the pretreated group (Group IV) decreased more significantly from 3.35 0.50 mEq/L to 1.81 0.41 mEq/L. 2) Pulse rate did not change significantly in groups that received continuous infusion of 7.5 units of RI (groups I and II) regardless of magnesium pretreatment, but increased significantly in groups injected with 15 units of RI (groups III and IV), pretreated or not. The pretreated group (group IV) had a more significant rise in pulse rate compared with the group that was not pretreated (group III). 3) In all of the groups, those pretreated with magnesium (groups II and IV) and those not pretreated (groups I and III), there was no significant change in systolic and diastolic blood pressures. Nor was arrhythmia detected. Conclusion: The above results indicate that while magnesium sulfate pretreatment at 30 mg/kg with insulin infusion affects serum potassium concentration, has an antiarrhythmic effect, and may induce tachycardia, it does not have any significant effect on blood pressure. (Korean J Anesthesiol 1998; 35: 839∼845)

Dietary Calcium Supplementation Prevents the Development of Hypertension in Deoxycorticosterone-Salt-Treated Dogs

High levels of dietary calcium attenuate the elevation of arterial pressure induced by deoxycorticosterone (DOC)-salt in trained, conscious dogs. This response resulted primarily from the failure of the expected rise in peripheral vascular resistance to develop. In addition, the enhanced pressor sensitivity to norepinephrine and angiotensin II associated with DOC-salt hypertension was normalized by high levels of dietary calcium. These changes could not be explained by changes in serum potassium concentration, plasma catecholamines concentration, or plasma volume. A possible explanation is that high levels of dietary calcium inhibit a parathyroid hypertensive factor that has been observed to be elevated in mineralocorticoid-induced hypertension. This hypothesis requires further studies.

Health status and the preoperative change in serum potassium concentration.

When evaluating preanaesthetic abnormal serum potassium (S-K) levels, the anaesthetist often relies upon blood tests performed on admission to hospital 1 or more days prior to surgery. However, the S-K is often altered between admission to hospital and the induction of anaesthesia. In this study, we examined the effects of health status and medication on the preoperative change in S-K concentration in 150 unselected elderly men awaiting urological operations. Oral daily medication was not given preoperatively on the day of surgery. One third of the patients showed a change of 0.4 mmol/l or more (range -1.1 to +1.2), with an increase as common as a decrease. Those on treatment with calcium-channel blockers or diuretics showed an increase in the S-K concentration in the preoperative period, while patients using oral antidiabetics showed a decrease. The use of beta-adrenoceptor antagonists was not a significant predictor of the change in S-K concentration. In conclusion, we found that alterations in serum potassium were common prior to surgery, but only a small fraction of this variance could be accounted for by health status and medication.

The effect of digoxin on the serum potassium concentration.

In recent studies on the influence of muscular and symphatoadrenergic activity on digoxin pharmacokinetics, the serum potassium concentration was found to increase during 2 h of supine rest in digitalized healthy subjects and out-patients. The present study was made in order to find out whether this change in serum potassium concentration is dependent on inhibition of the Na-K-ATPase activity by digitalis treatment. Ten healthy subjects were investigated on two separate occasions: before and after digitalization with digoxin 0.37-0.50 mg daily for 10 days. Serum potassium and digoxin concentrations were analysed before and after 2 h of rest in the sitting position. Without digoxin treatment, no change in serum potassium concentration was seen. During digoxin treatment, the serum potassium concentration increased by 0.19 +/- 0.23 mmol(l)-1 (p < 0.05) during the period of rest. Thus, a digitalis-induced depression of Na-K-ATPase activity seems to be a prerequisite for the described change in serum potassium concentration.

Anticancer effects of phytate

This study investigates the putative effect of potassium on energy expenditure. Eight young adult men were submitted to two different normocaloric mixed diets in a randomized order, containing either 163 +/- 9 or 69 +/- 2 mmol potassium/d. On the fifth day of each diet, after an overnight fast, resting metabolic rate (RMR) was measured over a 1-h period. After these measurements, either a potassium load (50 mmol) or a placebo were given to subjects submitted to the low- or the high-potassium diet, respectively. RMR was then measured again for 3 h and the last hour was kept for further analysis. Results showed that acute and chronic variations in potassium intake do not induce significant changes in RMR, and chronic but not acute changes in serum potassium concentration were significantly correlated with changes in energy expenditure (r = 0.74, P less than 0.05) by mechanisms that remain to be elucidated.

Human resting energy expenditure in relation to dietary potassium

This study investigates the putative effect of potassium on energy expenditure. Eight young adult men were submitted to two different normocaloric mixed diets in a randomized order, containing either 163 +/- 9 or 69 +/- 2 mmol potassium/d. On the fifth day of each diet, after an overnight fast, resting metabolic rate (RMR) was measured over a 1-h period. After these measurements, either a potassium load (50 mmol) or a placebo were given to subjects submitted to the low- or the high-potassium diet, respectively. RMR was then measured again for 3 h and the last hour was kept for further analysis. Results showed that acute and chronic variations in potassium intake do not induce significant changes in RMR, and chronic but not acute changes in serum potassium concentration were significantly correlated with changes in energy expenditure (r = 0.74, P less than 0.05) by mechanisms that remain to be elucidated.

Observed Changes in Serum Potassium Concentration following Repeat Centrifugation of Sarstedt Serum Gel Safety Monovettes after Storage

Observed Changes in Serum Potassium Concentration following Repeat Centrifugation of Sarstedt Serum Gel Safety Monovettes after Storage