sodium-bicarbonate and Hyperkalemia

Hyperkalemia is a common problem in both inpatients and outpatients. Many disease states (eg, chronic kidney disease) and medications may precipitate hyperkalemia. There are several drugs now available to treat hyperkalemia. Many of these drugs are relatively new. This review provides information regarding drug-induced causes of hyperkalemia and provides detailed information on the medications used to treat this problem.

Topics: Acute Disease; Administration, Intravenous; Adrenergic beta-Agonists; Arrhythmias, Cardiac; Calcium; Cation Exchange Resins; Chronic Disease; Electrocardiography; Glucose; Humans; Hyperkalemia; Hypoglycemia; Hypoglycemic Agents; Insulin; Polymers; Polystyrenes; Potassium; Silicates; Sodium Bicarbonate; Sodium Potassium Chloride Symporter Inhibitors

Hyperkalemia is a common electrolyte abnormality that can lead to life-threatening cardiac arrhythmia. Medical management of acute hyperkalemia revolves around three strategies-stabilizing the myocardium, intracellular shifting of serum potassium, and enhancing elimination of total body potassium via urinary or fecal excretion. In this review, we outline the current evidence behind the acute medical management of hyperkalemia.. Two new oral potassium-binding agents, patiromer and sodium zirconium cyclosilicate, show promise in the management of hyperkalemia. Their role in the acute setting needs further investigation. Recent investigations also suggest that the optimal dosing of intravenous insulin may be lower than previously described. Despite its prevalence, there is wide variability in the medical management of hyperkalemia in the acute setting. High-quality evidence demonstrating efficacy is lacking for many medications, though novel oral potassium-binding agents show promise. Overall, more research is necessary to establish optimal dosing strategies to manage hyperkalemia in the acute setting.

Topics: Acute Disease; Albuterol; Calcium; Diuretics; Humans; Hyperkalemia; Insulin; Polymers; Potassium; Silicates; Sodium Bicarbonate

Metabolic acidosis is a frequent complication of chronic kidney disease. Although it is known to appear at advanced stages, many studies suggest a state of "global protonic retention" starting at early stages of the disease, responsible of tissue damage, particularly musculoskeletal, alteration of protidic metabolism and endocrine disorders, promoting malnutrition and chronic inflammation, and finally increasing mortality. The majority of international recommandations suggest of supplementation by alkali, most of the time by sodium bicarbonate, to struggle against this complication. An interesting alternative to correct acidosis would consist on the modulation of the endogenous production of acid by playing with the alimentary incomes. In fact, it has been demonstrated that some different types of food produce or consume protons during their metabolism. Low protein diet and rich fresh fruits and vegetables diet would manage to correct at least as well as the supplementation by sodium bicarbonate the metabolic acidosis, and to struggle against its complications, noteworthy by slowing the decline of glomerular filtration rate by limiting the toxic adaptative fibrotic mechanisms, demonstrated by the decrease of urinary tubulo-interstitial suffering markers. Of the condition of being well led, those diets do not seem to expose patients to an over-risk of malnutrition or hyperkaliemia. They therefore appear to be an attractive alternative, efficiency and safe, to fight against chronic kidney disease metabolic acidosis and its complications.

Topics: Acidosis; Chronic Kidney Disease-Mineral and Bone Disorder; Combined Modality Therapy; Diet, Protein-Restricted; Dietary Proteins; Fruit; Humans; Hyperkalemia; Hypoalbuminemia; Inflammation; Malnutrition; Nutrition Policy; Protons; Renal Insufficiency, Chronic; Sarcopenia; Sodium Bicarbonate; Vegetables

Hyperkalemia is a common electrolyte disorder that can result in morbidity and mortality if not managed appropriately.. This review evaluates the classic treatments of hyperkalemia and discusses controversies and new medications for management.. Potassium (K+) plays a key role in determining the transmembrane potentials of "excitable membranes" present in nerve and muscle cells. K+ is the predominant intracellular cation, and clinical deterioration typically ensues when patients develop sufficiently marked elevation in extracellular fluid concentrations of K+ (hyperkalemia). Hyperkalemia is usually detected via serum clinical laboratory measurement. The most severe effect of hyperkalemia includes various cardiac dysrhythmias, which may result in cardiac arrest and death. Treatment includes measures to "stabilize" cardiac membranes, to shift K+ from extracellular to intracellular stores, and to promote K+ excretion. Calcium gluconate 10% dosed 10 mL intravenously should be provided for membrane stabilization, unless the patient is in cardiac arrest, in which case 10 mL calcium chloride is warranted. Beta-agonists and intravenous insulin should be given, and some experts recommend the use of synthetic short-acting insulins rather than regular insulin. Dextrose should also be administered, as indicated by initial and serial serum glucose measurements. Dialysis is the most efficient means to enable removal of excess K+. Loop and thiazide diuretics can also be useful. Sodium polystyrene sulfonate is not efficacious. New medications to promote gastrointestinal K+ excretion, which include patiromer and sodium zirconium cyclosilicate, hold promise.. Hyperkalemia can be deadly, and treatment requires specific measures including membrane stabilization, cellular shift, and excretion.

Topics: Acidosis; Buffers; Cation Exchange Resins; Dialysis; Drug Combinations; Electrocardiography; Glucose; Humans; Hyperkalemia; Hypoglycemia; Insulin; Polystyrenes; Potassium; Receptor, Insulin; Sodium Bicarbonate; Transcytosis; Treatment Outcome

Topics: Acute Disease; Adult; Albuterol; Biomarkers; Chi-Square Distribution; Down-Regulation; Glucose; Humans; Hyperkalemia; Insulin; Odds Ratio; Potassium; Sodium Bicarbonate; Treatment Outcome

Topics: Adrenergic beta-Agonists; Aldosterone; Diagnosis, Differential; Gluconates; Humans; Hyperkalemia; Hypokalemia; Insulin; Kidney Tubules; Potassium; Renal Dialysis; Sodium Bicarbonate

Topics: Adrenergic beta-Agonists; Cation Exchange Resins; Humans; Hyperkalemia; Hypoglycemic Agents; Insulin; Sodium Bicarbonate

Non-oliguric hyperkalaemia is a common and serious complication of extreme prematurity, resulting from a potassium loss from the intra- into the extracellular space during a specific post-natal period. Treatment of this disorder has been adapted from the treatment of hyperkalaemia in renal failure, an entity of completely different pathophysiology. A few years ago, the administration of salbutamol, which induces cellular potassium uptake, was proposed as a new therapeutic option. In this review article we discuss the pathogenesis and current therapy of non-oliguric hyperkalaemia of the premature infant, with special emphasis on the presently available knowledge and concerns with regard to the use of salbutamol. Being aware of the paucity of studies on non-oliguric hyperkalaemia, we propose treatment recommendations which are based on best available evidence. These comprise the administration of calcium, infusion of insulin plus glucose, correction of acidosis, and exchange transfusion or peritoneal dialysis as a last resort therapy. Before controlled trials on efficacy of salbutamol treatment of non-oliguric hyperkalaemia of the premature infant can be initiated, more data on safety are needed.

Topics: Adrenergic beta-Agonists; Albuterol; Calcium; Diuretics; Evidence-Based Medicine; Exchange Transfusion, Whole Blood; Glucose; Humans; Hyperkalemia; Hypoglycemic Agents; Infant, Newborn; Infant, Premature, Diseases; Insulin; Neonatology; Peritoneal Dialysis; Practice Guidelines as Topic; Risk Factors; Safety; Sodium Bicarbonate; Treatment Outcome

The foremost step in the initial clinical management of hyperkalemia is to decide whether a hyperkalemic patient requires immediate treatment to avoid a life-threatening situation (serum potassium concentration >6.0 mEq/l and EKG changes). When the decision for urgent treatment of hyperkalemia is based on EKG changes, an important caveat for clinicians is that absent or atypical EKG changes do not exclude the necessity for immediate intervention. Once an urgent situation has being handled with intravenous push of a 10% calcium salt, the initiation of short-term measures can be launched by either a single or combined regimen of the three agents that cause a transcellular shift of potassium - insulin with glucose, beta(2)-agonist (albuterol), and NaHCO(3). As the first choice among these available options, we favor an intravenous bolus of 10 units of insulin with 50 ml of 50% glucose alone or in combination with 10-20 mg of albuterol by nebulizer. These can be repeated as required until the institution of hemodialysis. The combination of insulin with glucose and NaHCO(3) as an another option needs further clarification for its additive effects. However, NaHCO(3) has lost its favor because of its poor efficacy as a potassium-lowering agent when used alone. The next step is to remove potassium from the body - diuretics (furosemide), cation exchange resin (kayexelate) with sorbitol, and dialysis (preferably hemodialysis). The final important step for the managements of hyperkalemia is a long-term plan to prevent its recurrence or worsening. In addition to every effort to elucidate underlying causes and pathophysiologic mechanisms for hyperkalemia, an extensive search must be made to uncover overt or sometimes covert medications that may have led to the development of hyperkalemia. Furthermore, one must obtain detailed dietary and medical history of hyperkalemic patients.

Topics: Adrenergic beta-Agonists; Albuterol; Calcium; Digestive System; Drug Therapy, Combination; Electrocardiography; Humans; Hyperkalemia; Insulin; Kidney; Potassium; Renal Dialysis; Sodium Bicarbonate

Topics: Animals; Catecholamines; Emergency Service, Hospital; Humans; Hyperkalemia; Insulin; Kidney Failure, Chronic; Potassium; Practice Guidelines as Topic; Renal Dialysis; Sodium Bicarbonate

Topics: Acidosis; Acidosis, Lactic; Acidosis, Respiratory; Animals; Dogs; Guidelines as Topic; Humans; Hyperkalemia; India; Infant, Newborn; Sodium Bicarbonate; Tromethamine

Topics: Calcium Gluconate; Glucose; Humans; Hyperkalemia; Hypokalemia; Insulin; Kidney; Polystyrenes; Potassium; Sodium Bicarbonate

Tubular acidosis is diagnosed when hyperchloremic acidosis is associated with inappropriate NH4 excretion (less than or equal to 40 mmol/24 hours). Urinary pH is variable because it depends on the secretion of H+ into the collecting duct and is inversely correlated with the amount of ammonia available in the urine. Administration of NaHCO3 for diagnostic purpose allows to eliminate proximal tubular acidosis and to measure the elevation of urinary PCO2 reflecting the secretion of H+ in the collecting duct. Hypokalemia points towards distal tubular acidosis, either by defect of H(+)-ATPases pumps, or by the incapacity to create a normal gradient of H+. In contrast hyperkalemia suggests distal tubular acidosis associated either with hypoaldosteronism or with diminution of trans-epithelial voltage or with pseudohypoaldosteronism. The incidence of distal tubular acidosis with hyperkalemia is increasing whereas distal tubular acidosis with hypokalemia remain rare.

Topics: Acidosis, Renal Tubular; Bicarbonates; Humans; Hyperkalemia; Hypokalemia; Sodium; Sodium Bicarbonate

Topics: Adrenergic beta-Agonists; Bicarbonates; Calcium; Glucose; Humans; Hyperkalemia; Insulin; Sodium; Sodium Bicarbonate

Topics: Adolescent; Adult; Aldosterone; Bicarbonates; Blood Pressure; Child; Diet, Sodium-Restricted; Diuretics; Female; Glomerular Filtration Rate; Humans; Hyperkalemia; Hypertension; Kidney Tubules; Male; Mannitol; Middle Aged; Mineralocorticoids; Potassium; Renin; Sodium; Sodium Bicarbonate; Syndrome

Mechanisms of renal potassium excretion and internal potassium balance as the main determinants of serum and/or total body potassium are discussed. Renal handling of potassium is reviewed, with particular attention to the effects of diuretics, acid-base disturbances and aldosterone-deficient states. Among the regulatory processes of internal potassium balance, the importance of adrenergic stimuli/drugs, of acid-base balance, and of magnesium and insulin is stressed. Physiologic and pathophysiologic evidence provides the basis for discussion of relevant clinical implications.

Topics: Acid-Base Equilibrium; Adult; Aged; Alkalosis; Bicarbonates; Biological Transport; Catecholamines; Chlorides; Diuretics; Female; Humans; Hyperkalemia; Hypokalemia; Insulin; Kidney; Kidney Tubules; Magnesium Deficiency; Male; Middle Aged; Potassium; Renin-Angiotensin System; Sodium; Sodium Bicarbonate; Stress, Physiological

Acidemia and electrolyte imbalances such as hyperkalemia are common in neonatal calves with diarrhea. Acidemia negatively affects the cellular response to insulin and may therefore result in deranged glucose, potassium, and phosphorus homeostasis. The primary aim of this study was to compare indices that characterize the dynamic glucose and insulin response between acidemic and nonacidemic neonatal diarrheic calves and a healthy control group during an intravenous glucose tolerance test (IVGTT) that consisted of i.v. administration of 0.3 g of glucose per kg of body weight. Secondary aims were to characterize the associated changes in plasma potassium and phosphorus concentrations. The effect of correction of profound acidemia with a sodium bicarbonate containing infusion on these parameters was also assessed. Thirty calves (age ≤21 d) were purposively assigned to one of the following groups: 10 calves with diarrhea and profound acidemia (venous blood pH <7.20) where an IVGTT was performed before and after treatment with sodium bicarbonate, 10 calves with diarrhea and minimal acid-base disturbance (venous blood pH >7.35), and 10 healthy control calves. Profoundly acidemic diarrheic calves (jugular venous blood pH 6.99 ± 0.10) had a similar initial increase in plasma insulin concentration to that in healthy control calves or nonacidemic calves with diarrhea. However, insulin concentrations remained relatively stable in acidemic calves between 15 and 60 min after the start of the IVGTT, whereas a marked decrease in plasma insulin concentrations occurred in all other groups during the same period of time. We conclude that acidemia does not alter cell glucose availability or the dynamic response of glucose, phosphorus, and potassium to insulin; however, acidemia markedly prolongs plasma insulin concentrations following an IVGTT through an unidentified mechanism. Results of this study emphasize the importance of correcting acidemia and metabolic acidosis in neonatal calves with diarrhea.

Topics: Acidosis; Animals; Animals, Newborn; Cattle; Cattle Diseases; Diagnostic Tests, Routine; Diarrhea; Glucose; Glucose Tolerance Test; Hyperkalemia; Insulin; Phosphorus; Phosphorus, Dietary; Potassium; Sodium Bicarbonate

To determine whether time to prepare IV medications for hyperkalemia varied by 1) drug, 2) patient weight, 3) calcium salt, and 4) whether these data support the Advanced Cardiac Life Support recommended sequence.. Prospective randomized simulation-based study.. Single pediatric tertiary medical referral center.. Pediatric nurses and adult or pediatric pharmacists.. Subjects were randomized to prepare medication doses for one of four medication sequences and stratified by one of three weight categories representative of a neonate/infant, child, or adult-sized adolescent: 4, 20, and 50 kg. Using provided supplies and dosing references, subjects prepared doses of calcium chloride, calcium gluconate, sodium bicarbonate, and regular insulin with dextrose. Because insulin and dextrose are traditionally prepared and delivered together, they were analyzed as one drug. Subjects preparing medications were video-recorded for the purpose of extracting timing data.. A total of 12 nurses and 12 pharmacists were enrolled. The median (interquartile range) total preparation time for the three drugs was 9.5 minutes (6.4-13.7 min). Drugs were prepared significantly faster for larger children (50 kg, 6.8 min [5.6-9.1 min] vs 20 kg, 9.5 min [8.6-13.0 min] vs 4 kg, 16.3 min [12.7-18.9 min]; p = 0.001). Insulin with dextrose took significantly longer to prepare than the other medications, and there was no difference between the calcium salts: (sodium bicarbonate, 1.9 [0.8-2.6] vs calcium chloride, 2.1 [1.2-3.1] vs calcium gluconate, 2.4 [2.1-3.0] vs insulin with dextrose, 5.1 min [3.7-7.7 min], respectively; p < 0.001). Forty-two percent of subjects (10/24) made at least one dosing error.. Medication preparation for hyperkalemia takes significantly longer for smaller children and preparation of insulin with dextrose takes the longest. This study supports Pediatric Advanced Life Support guidelines to treat hyperkalemia during pediatric cardiac arrest similar to those recommended per Advanced Cardiac Life Support (i.e., first, calcium; second, sodium bicarbonate; and third, insulin with dextrose).

Topics: Adolescent; Advanced Cardiac Life Support; Body Weight; Calcium Chloride; Calcium Gluconate; Child; Child, Preschool; Critical Care; Drug Compounding; Female; Glucose; Heart Arrest; Humans; Hyperkalemia; Infant; Infant, Newborn; Insulin; Male; Prospective Studies; Sodium Bicarbonate; Time Factors; Water-Electrolyte Balance

Ten patients with acute and 60 with chronic renal failure (both groups having hyperkalaemia), were managed at Kenyatta National Hospital in the medical wards and Renal Unit between August, 1995 and January, 1996. They were divided into seven different treatment groups, each consisting of ten patients. Treatment A glucose 25g i.v. with insulin 10 units i.v., treatment B 50 mmol of 8.4% sodium bicarbonate infusion, treatment C 0.5mg of salbutamol i.v. in 50mls 5% dextrose, treatment D was a combination of treatments A and B, treatment E was a combination of treatment B and C, treatment F was a combination of treatments A and C while treatment G was a combination of treatments A and B and C. Serum potassium was measured, 30 minutes, 1 hour, 2 hours, 4 hours and 8 hours after treatment. Plasma glucose concentration was measured before treatment was given and 1 hour after in all patients. Electrocardiography was done before treatment on all patients and repeated 30 minutes and 1 hour after treatment for the patients with hyperkalaemic changes on the initial recording. All treatment modalities had satisfactory potassium lowering effects. Of the single therapeutic approaches, treatment A and C were equieffective, but better than treatment B (P < 0.001). Amongst the two regimen combinations, treatment D and F were more efficacious than treatment E and all the single therapeutic approaches (P < 0.001). Treatment G was the most efficacious in lowering serum potassium in this study. All treatment modalities had maximum serum potassium lowering effect at 1-2 hours. A fall in plasma glucose concentration was a notable feature of treatments A and D, but significant hypoglycaemia occurred in 20% of patients receiving treatment A and in none on treatment D. The ECG changes of hyperkalaemia did not correlate with serum potassium levels. The normalisation of hyperkalaemic ECG alteration occurred within the first 30 minutes after treatment. In conclusion, combination therapies for hyperkalaemia appear to be more efficacious than single therapeutic approaches. Inclusion of salbutamol seems to protect against insulin induced hypoglycaemia. The maximum potassium lowering effect is observed 1-2 hours of administration of either agents. The potassium reducing effect remains significant compared to baseline values even after 8 hours. If dialysis cannot be instituted early enough it seems reasonable to repeat treatment every 4-6 hours to sustain the effect. Repeated administration

Topics: Acute Kidney Injury; Adolescent; Adrenergic beta-Agonists; Adult; Aged; Aged, 80 and over; Albuterol; Drug Therapy, Combination; Electrocardiography; Glucose Solution, Hypertonic; Humans; Hyperkalemia; Hypoglycemic Agents; Infusions, Intravenous; Insulin; Kidney Failure, Chronic; Middle Aged; Prospective Studies; Single-Blind Method; Sodium Bicarbonate; Sodium-Potassium-Exchanging ATPase

Acute treatment of hyperkalemia in patients with end-stage renal disease requires temporizing measures to shift potassium rapidly from the extracellular to the intracellular fluid compartments until hemodialysis can be initiated. Whereas insulin and albuterol are effective in lowering plasma potassium acutely, bicarbonate by itself is not. Bicarbonate administration may, however, potentiate the effects of insulin and albuterol on plasma potassium. Using a prospective cross-over design, we investigated the acute effects of (1) isotonic bicarbonate, (2) isotonic saline, (3) insulin + bicarbonate, (4) insulin + saline, (5) albuterol + bicarbonate, and (6) albuterol + saline on plasma potassium as well as blood bicarbonate and pH in nondiabetic hemodialysis patients. After obtaining a baseline blood sample, the subjects received one of the six treatment protocols, with plasma potassium measured every 15 minutes over 1 hour. Neither isotonic bicarbonate nor isotonic saline decreased plasma potassium significantly (-0.03 +/- 0.06 mmol/L v -0.01 +/- 0.10 mmol/L at 60 minutes; P = 0.60). Intravenous insulin decreased plasma potassium by a similar degree when given in conjunction with bicarbonate or saline (-0.81 +/- 0.05 mmol/L v -0.85 +/- 0.06 mmol/L at 60 minutes; P = 0.65). Likewise, nebulized albuterol decreased plasma potassium by a similar degree when given with bicarbonate or saline (-0.71 +/- 0.16 mmol/L v -0.53 +/- 0.15 mmol/L at 60 minutes; P = 0.18). The three protocols that included bicarbonate administration resulted in significant increases in blood bicarbonate (P < 0.005) and pH (P < 0.01), whereas the three protocols that included saline did not affect blood bicarbonate or pH. These observations suggest that bicarbonate administration does not potentiate the potassium-lowering effects of insulin or albuterol in hemodialysis patients.

Topics: Adrenergic beta-Agonists; Adult; Aged; Albuterol; Cross-Over Studies; Drug Synergism; Female; Humans; Hydrogen-Ion Concentration; Hyperkalemia; Insulin; Kidney Failure, Chronic; Male; Middle Aged; Potassium; Prospective Studies; Renal Dialysis; Sodium Bicarbonate

To survey treatment and prognosis of hyperkalemia patients in the emergency department and to analyze factors associated with all-cause in-hospital mortality.. A total of 579 patients [median age 64 (22) years; 310 men (53.5%) and 269 women (46.5%)] with hyperkalemia were enrolled, among which, 317 (54.7%), 143 (24.7%) and 119 (20.6%) were mild, moderate, and severe hyperkalemia, respectively. 499 (86.20%) patients received potassium-lowering therapy, forty-four treatment regimens were administered. Insulin and glucose (I+G, 61.3%), diuretics (Diu, 57.2%), sodium bicarbonate (SB, 41.9%) and calcium gluconate/chloride (CA, 44.4%) were commonly used for the treatment of hyperkalemiain the emergency department. The combination of insulin and glucose, calcium gluconate/chloride, diuretics and sodium bicarbonate (I+G+CA+Diu+SB) was the most favored combined treatment regimen of hyperkalemia in the emergency department. The higher serum potassium concentration, the higher proportion of administrating combined treatment regimen and/or hemodialysis (HD) (the proportion of administrating combined treatment regimen in mild, moderate, and severe hyperkalemia patients were 58.4%, 82.5% and 94.8%; the proportion of administrating HD in mild, moderate, and severe hyperkalemia patients were 9.7%, 13.3% and 16.0%, respectively). The proportion of achievement of normokalaemia elevated as the kinds of potassium lowering treatment included in the combined treatment regimen increased. The proportion of achievement of normokalaemia was 100% in the combined treatment regimen including 6 kinds of potassium lowering therapy. Among various potassium lowering treatments, HD contributed to the highest rate of achievement of normokalaemia (93.8%). 111 of 579 (19.20%) hyperkalemia patients died in hospital. Cox regression model revealed that complicated with cardiac dysfunction predicted higher mortality [hazard ratio (HR) = 1.757, 95% confidence interval (95%CI) was 1.155-2.672, P = 0.009]. Achievement of normokalaemia and administration of diuretics attributed to lower mortality (HR = 0.248, 95%CI was 0.155-0.398, P = 0.000; HR = 0.335, 95%CI was 0.211-0.531, P = 0.000, respectively).. Treatment of hyperkalemia in the emergency department were various. Complicated with cardiac dysfunction were associated with higher mortality. Achieving normokalaemia was associated with decreased mortality.

Topics: Adolescent; Calcium Gluconate; Chlorides; Diuretics; Emergency Service, Hospital; Female; Glucose; Humans; Hyperkalemia; Insulin; Male; Middle Aged; Potassium; Prognosis; Sodium Bicarbonate

Topics: Bicarbonates; Humans; Hydrogen-Ion Concentration; Hyperkalemia; Potassium; Sodium Bicarbonate

Sodium zirconium cyclosilicate (SZC) binds potassium and ammonium in the gastrointestinal tract. In addition to serum potassium reduction, Phase 2 trial data have shown increased serum bicarbonate with SZC, which may be clinically beneficial because maintaining serum bicarbonate ≥22 mmol/L preserves kidney function. This exploratory analysis examined serum bicarbonate and urea, and urine pH data from three SZC randomized, placebo-controlled Phase 3 studies among patients with hyperkalaemia [ZS-003 (n = 753), HARMONIZE (n = 258) and HARMONIZE-Global (n = 267)].. In all studies, patients received ≤10 g SZC 3 times daily (TID) for 48 h to correct hyperkalaemia, followed by randomization to maintenance therapy with SZC once daily (QD) versus placebo for ≤29 days among those achieving normokalaemia.. Significant dose-dependent mean serum bicarbonate increases from baseline of 0.3 to 1.5 mmol/L occurred within 48 h of SZC TID in ZS-003 (all P < 0.05), which occurred regardless of chronic kidney disease (CKD) stage. Similar acute increases in HARMONIZE and HARMONIZE-Global were maintained over 29 days. With highest SZC maintenance doses, patient proportions with serum bicarbonate <22 mmol/L fell from 39.4% at baseline to 4.9% at 29 days (P = 0.005) in HARMONIZE and from 87.9% to 70.1%, (P = 0.006) in HARMONIZE-Global. Path analyses demonstrated that serum urea decreases (but not serum potassium or urine pH changes) were associated with SZC effects on serum bicarbonate.. SZC increased serum bicarbonate concentrations and reduced patient proportions with serum bicarbonate <22 mmol/L, likely due to SZC-binding of gastrointestinal ammonium. These SZC-induced serum bicarbonate increases occurred regardless of CKD stage and were sustained during ongoing maintenance therapy.

Topics: Bicarbonates; Blood Urea Nitrogen; Gastrointestinal Tract; Humans; Hyperkalemia; Male; Middle Aged; Potassium; Renal Insufficiency, Chronic; Silicates; Sodium Bicarbonate; Urea

Malignant hyperthermia is defined in the International Classification of Diseases as a progressive life-threatening hyperthermic reaction occurring during general anaesthesia. Malignant hyperthermia has an underlying genetic basis, and genetically susceptible individuals are at risk of developing malignant hyperthermia if they are exposed to any of the potent inhalational anaesthetics or suxamethonium. It can also be described as a malignant hypermetabolic syndrome. There are no specific clinical features of malignant hyperthermia and the condition may prove fatal unless it is recognised in its early stages and treatment is promptly and aggressively implemented. The Association of Anaesthetists has previously produced crisis management guidelines intended to be displayed in all anaesthetic rooms as an aide memoire should a malignant hyperthermia reaction occur. The last iteration was produced in 2011 and since then there have been some developments requiring an update. In these guidelines we will provide background information that has been used in updating the crisis management recommendations but will also provide more detailed guidance on the clinical diagnosis of malignant hyperthermia. The scope of these guidelines is extended to include practical guidance for anaesthetists dealing with a case of suspected malignant hyperthermia once the acute reaction has been reversed. This includes information on care and monitoring during and after the event; appropriate equipment and resuscitative measures within the operating theatre and ICU; the importance of communication and teamwork; guidance on counselling of the patient and their family; and how to make a referral of the patient for confirmation of the diagnosis. We also review which patients presenting for surgery may be at increased risk of developing malignant hyperthermia under anaesthesia and what precautions should be taken during the peri-operative management of the patients.

Topics: Acidosis; Body Temperature; Calcium; Carbon Dioxide; Compartment Syndromes; Dantrolene; Disseminated Intravascular Coagulation; Heart Rate; Humans; Hyperkalemia; Malignant Hyperthermia; Muscle Relaxants, Central; Myoglobinuria; Pulmonary Ventilation; Risk Factors; Sodium Bicarbonate

Hyperkalemia is an electrolyte disorder commonly encountered in the emergency department that can result in significant morbidity and mortality. While sodium bicarbonate is often used for acute lowering of serum potassium, its efficacy is not well established. The purpose of this study was to evaluate and quantify the amount of potassium reduction in emergency department patients who received intravenous sodium bicarbonate as part of treatment for hyperkalemia compared with those who did not.. A retrospective electronic chart review was conducted on adult patients who presented to the emergency department with initial potassium concentration greater than or equal to 5.4 mMol/L and received intravenous insulin as part of hyperkalemia treatment. Patients who received intravenous sodium bicarbonate in addition to intravenous insulin were included in the sodium bicarbonate group. The control group included patients who did not receive intravenous sodium bicarbonate. The primary objective of this study was to compare the absolute reduction in serum potassium between initial and second concentrations in patients from the sodium bicarbonate group and those in the control group.. A total of 106 patients were included in this study with 38 patients in the sodium bicarbonate group and 68 patients in the control group. Median initial potassium concentration was 6.6 mMol/L in the sodium bicarbonate group and 6.1 mMol/L in the control group (P = 0.009). Absolute reduction of potassium at first repeat was 1 and 0.9 mMol/L in sodium bicarbonate group and control group respectively (P = 0.976).. The addition of sodium bicarbonate therapy to intravenous insulin in the treatment of hyperkalemia did not offer statistically significant added efficacy in potassium lowering. Larger studies are needed to further validate the result findings.

Topics: Case-Control Studies; Emergency Service, Hospital; Female; Humans; Hyperkalemia; Male; Middle Aged; Potassium; Retrospective Studies; Sodium Bicarbonate

Atypical hemolytic uremic syndrome (aHUS) is a complement-mediated disease manifesting in thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury. It has a higher incidence of extrarenal manifestations, including central nervous system findings like seizure or stroke, pancreatitis, and cardiac manifestations.. We present a case of an unimmunized 14-month-old girl presenting with generalized seizure and ultimately diagnosed with aHUS. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: These atypical neurological symptoms can cause the diagnosis to be commonly missed in the emergency department. The etiology of approximately 60% of patients with aHUS can be attributed to genetic mutations in complement regulators including factor H, membrane cofactor protein, factor I, activator factor B, or C3. Although previously treated with plasma transfusion and immunosuppressants, eculizumab is a newer treatment that has been changing prognosis and management of aHUS, but it should be administered within 48 h of symptom onset for best efficacy.

Topics: Atypical Hemolytic Uremic Syndrome; Buffers; Calcium Gluconate; Electroencephalography; Female; Humans; Hyperkalemia; Hypnotics and Sedatives; Incidence; Infant; Midazolam; Seizures; Sodium Bicarbonate; Thrombocytopenia; Vomiting

Bradycardia is a common vital sign encountered in the emergency department. These patients are often hemodynamically stable and require no emergent intervention. On occasion, bradycardia can cause hemodynamic instability, and there are established treatment pathways involving atropine, ionotropic and vasopressive infusions, and eventual mechanical pacing, if necessary. However, these pathways fail to account for the many and varied causes of bradycardia and their treatment.. A 24-year-old man presented to our emergency department with syncope caused by symptomatic bradycardia. This was caused by a largely unrecognized synergistic bradycardia resulting from renal failure, AV nodal blocker use, and hyperkalemia. Our patient's worsening renal failure caused accumulation of both potassium and beta blocker, which resulted in bradycardia and hypotension, in turn worsening renal failure secondary to poor renal perfusion and potentiating his hyperkalemia and beta blocker toxicity. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: There is a growing number of cases that suggest this is an underrecognized synergistic and potentially lethal mechanism of hemodynamically unstable bradycardia and the treatment falls outside of typical algorithms for handling bradycardia. Understanding the multiple causes of these patients' hemodynamically unstable bradycardia allows for maximal medical management and can prevent unnecessary invasive management for these patients.

Topics: Adrenergic beta-Antagonists; Bradycardia; Calcium Gluconate; Electrocardiography; Emergency Service, Hospital; Fluid Therapy; Humans; Hyperkalemia; Male; Renal Insufficiency; Sodium Bicarbonate; Young Adult

Emergency department (ED) treatment of hyperkalemia often involves shifting potassium into the intracellular space. There is uncertainty whether transcellular shifting causes insufficient potassium removal during hemodialysis, resulting in a subsequent need for further medical therapy or multiple sessions of hemodialysis.. We sought to determine whether transcellular potassium shifting in ED patients with hyperkalemia who undergo hemodialysis is associated with recurrent hyperkalemia with or without repeat hemodialysis within 24 h.. This was a retrospective observational study of ED patients with a potassium value > 5.3 mmol/L and ≥1 hemodialysis run. Transcellular shifting medications were defined as albuterol, insulin, and sodium bicarbonate. Primary outcomes were recurrent hyperkalemia with and without repeat hemodialysis within 24 h of the initial dialysis run. Generalized estimating equation models were created for the outcomes using administration of a shifting medication as the primary predictor.. Four hundred seventy-nine encounters were identified. In 238 (50%) encounters, a shifting medication was administered. There were 85 outcomes of recurrent hyperkalemia and 36 outcomes of recurrent hyperkalemia with repeat hemodialysis. After adjustment, administration of shifting medications was not associated with recurrent hyperkalemia (adjusted odds ratio 1.26, 95% confidence interval 0.71-2.23) or recurrent hyperkalemia with repeat dialysis (adjusted odds ratio 1.90, 95% confidence interval 0.80-4.48).. Administration of transcellular shifting medications for hyperkalemia in the ED was not associated with either recurrent hyperkalemia after hemodialysis or the need for a second dialysis session within 24 h. Our findings address the uncertainty regarding transcellular potassium shifting before emergent dialysis and support safe ED administration of medications that shift potassium to the intracellular space.

Topics: Albuterol; Dialysis; Emergency Service, Hospital; Female; Humans; Hyperkalemia; Insulin; Male; Middle Aged; Potassium; Retrospective Studies; Sodium Bicarbonate; Transcellular Cell Migration

Topics: Anticoagulants; Diuretics; Heparin; Humans; Hyperkalemia; Potassium; Potassium, Dietary; Renal Insufficiency, Chronic; Renin-Angiotensin System; Severity of Illness Index; Sodium Bicarbonate; Sodium, Dietary

Calcium and sodium bicarbonate (SB) are frequently used in treating patients with severe hyperkalaemia. We evaluated the efficacy of these medications for the treatment of severe hyperkalaemia during cardiopulmonary resuscitation (CPR). We also hypothesised that the effects of these medications might be associated with serum potassium level during CPR.. We conducted a retrospective observational study in a single medical centre. From adult patients who had suffered an in-hospital cardiac arrest from 2006 through 2012, we included those with a serum potassium level>6.5 mEq/L measured during CPR. We used multivariable logistic regression analysis to study the association of calcium/SB with sustained return of spontaneous circulation (ROSC).. Among the 109 patients included in our analysis, 40 (36.7%) patients achieved sustained ROSC, and only four (3.7%) patients survived to hospital discharge. The mean serum potassium level was 7.8 mEq/L. The analysis indicated that administration of SB was positively associated with sustained ROSC when serum potassium level was <7.9 mEq/L (odds ratio [OR]: 10.51; 95% confidence interval [CI]: 1.50-112.89; p: 0.03); administration of calcium and SB was also positively associated with sustained ROSC when serum potassium level was <9.4 mEq/L (OR: 51.11; 95% CI: 3.12-1639.16; p: 0.01).. The use of calcium and SB might be effective in the treatment of severe hyperkalaemia during cardiac arrest. The efficacy of SB/calcium correlated with serum potassium level. However, because the number of patients included in the analysis was small, this conclusion should be further examined in the future.

Topics: Adult; Aged; Calcium; Cardiopulmonary Resuscitation; Female; Heart Arrest; Humans; Hyperkalemia; Inpatients; Male; Middle Aged; Retrospective Studies; Sodium Bicarbonate; Taiwan; Treatment Outcome

Topics: Calcium; Cardiopulmonary Resuscitation; Heart Arrest; Humans; Hyperkalemia; Sodium Bicarbonate

Loperamide, a non-prescription anti-diarrheal agent, is a peripheral mu-opioid receptor agonist that is excluded from the blood-brain barrier by p-glycoprotein at therapeutic doses. Overdoses of loperamide penetrate the central nervous system (CNS), leading to abuse. We report cardiac conduction abnormalities and dysrhythmias after ingestion of a recreational supra-therapeutic dose of loperamide confirmed with an elevated blood loperamide concentration.. A 48-year-old woman with a history of alcohol and benzodiazepine abuse presented to the emergency department (ED) with somnolence, weakness and slurred speech. She was taking 20 to 40 tablets of 2 mg loperamide 1-2 times/day for weeks along with clonazepam and whiskey. Vital signs were: blood pressure (BP), 124/90 mmHg; heart rate (HR), 88/min; respiratory rate(RR), 20/min; T, 36.9 °C; O2 saturation 100% on room air (RA). Glucose was 6.4 mmol/L. Electrocardiogram (ECG) had a ventricular rate of 58/min, QRS 164 ms, QT 582 ms with no discernable p-waves. Lactate was 3.5 mmol/L and potassium was 6.2 mEq/L. Labs were notable for an anion gap of 20 mEq/L, ethanol of 3.9 mmol/L, creatinine of 2.3 mg/dL and loperamide concentration of 210 ng/mL (average therapeutic plasma concentration 1.2 ng/mL). She became hypotensive, but responded to fluids. Following treatment for hyperkalemia with calcium, insulin, dextrose, and hypertonic sodium bicarbonate a repeat ECG had a ventricular rate of 66/min, QRS 156 ms, and QT 576 ms. Magnesium was given and pacer pads were placed. During the infusion of magnesium, her BP fell to 92/58 mmHg with a HR of 54/min, RR 14/min, O2 saturation of 97% on RA so the infusion was stopped. The ECG after the magnesium infusion had a ventricular rate of 51/min, QRS of 134 ms, and QT 614 ms. In the ICU she had multiple runs of non-sustained ventricular tachycardia that did not require therapy. Over the next 48 h she improved and was transferred to a floor bed. On day four of hospitalization the patient left against medical advice. At that time, her ECG showed sinus tachycardia with a heart rate 114/min, QRS 82 ms, QT 334 ms.. Loperamide produces both QRS and QT prolongation at supra-therapeutic dosing. A blood loperamide concentration of 210 ng/mL is among the highest concentrations reported. Supra-therapeutic dosing of loperamide is promoted on multiple drug-use websites and online forums as a treatment for opioid withdrawal, as well as for euphoric effects. With the current epidemic of prescription opioid abuse, toxicity related to loperamide, an opioid agonist that is readily available without a prescription is occurring more frequently. It is important for clinicians to be aware of the potentially life-threatening toxicity related to loperamide abuse in order to provide proper diagnosis, management and patient education.

Topics: Alcoholism; Arrhythmias, Cardiac; Benzodiazepines; Blood Pressure; Calcium; Central Nervous System; Clonazepam; Dose-Response Relationship, Drug; Drug Overdose; Electrocardiography; Emergency Service, Hospital; Female; Glucose; Heart Rate; Humans; Hyperkalemia; Insulin; Loperamide; Magnesium; Middle Aged; Respiratory Rate; Sodium Bicarbonate; Substance-Related Disorders

Irreversible electroporation is a fast-growing liver ablation technique. Although safety has been well documented in small ablations, our aim is to assess its safety and feasibility when a large portion of liver is ablated. Eighty-seven mice were subjected to high voltage pulses directly delivered across parallel plate electrodes comprising around 40% of mouse liver. One group consisted in 55 athymic-nude, in which a tumor from the KM12C cell line was grown and the other thirty-two C57-Bl6 non-tumoral mice. Both groups were subsequently divided into subsets according to the delivered field strength (1000 V/cm, 2000 V/cm) and whether or not they received anti-hyperkalemia therapy. Early mortality (less than 24 hours post-IRE) in the 2000 V/cm group was observed and revealed considerably higher mean potassium levels. In contrast, the animals subjected to a 2000 V/cm field treated with the anti-hyperkalemia therapy had higher survival rates (OR = 0.1, 95%CI = 0.02-0.32, p < 0.001). Early mortality also depended on the electric field magnitude of the IRE protocol, as mice given 1000 V/cm survived longer than those given 2000 V/cm (OR = 4.7, 95%CI = 1.8-11.8, p = 0.001). Our findings suggest that ionic disturbances, mainly due to potassium alterations, should be warned and envisioned when large volume ablations are performed by IRE.

Topics: Albuterol; Animals; Cell Membrane Permeability; Electrochemotherapy; Furosemide; Hyperkalemia; Liver; Liver Neoplasms, Experimental; Male; Mice; Mice, Inbred C57BL; Mice, Nude; Organ Size; ROC Curve; Sodium Bicarbonate

Topics: Bicarbonates; Humans; Hyperkalemia; Potassium; Sodium; Sodium Bicarbonate

Topics: Acute Kidney Injury; Adult; Aged; Calcium Gluconate; Female; Glycine; Glyphosate; Herbicides; Humans; Hyperkalemia; Male; Middle Aged; Plasmapheresis; Severity of Illness Index; Sodium Bicarbonate; Suicide, Attempted; Treatment Outcome

Chronic hemodialysis patients undergoing surgery require intensive care. The purpose of this study was to determine the incidence and risk factors of emergency treatment before the planned elective postoperative dialysis.. One hundred and ten dialysis patients undergoing elective noncardiac surgery were retrospectively analyzed.. Emergency treatment was performed in 31 (28.1%) of the 110 patients, including one patient with emergency dialysis, because of hyperkalemia (n = 27) or metabolic acidosis (n = 4). Receiving operating characteristic curve analysis showed a cutoff value for serum potassium concentration < 4.0 mEq x l(-1) estimated by maximizing the Youden index. We could not find other perioperative data as significant risk factors for emergency treatment.. About 30 percent of dialysis patients aftet elective noncardiac surgery required emergency treatment. The highest risk was high serum potassium concentrations after induction of anesthesia Preoperative serum potassium concentrations should be kept below 4.0 mEq x l(-1) to avoid postoperative emergency treatment.

Topics: Aged; Calcium Chloride; Dialysis; Elective Surgical Procedures; Emergency Medical Services; Female; Humans; Hyperkalemia; Incidence; Intensive Care Units; Male; Middle Aged; Perioperative Care; Postoperative Care; Postoperative Complications; Retrospective Studies; Risk Factors; Sodium Bicarbonate; Surgical Procedures, Operative; Time Factors

The aim of this study was to determine the incidence of treatment of hyperkalemia in hospitalized patients.. This is a prospective chart review of adults in a tertiary care hospital with hyperkalemia (serum potassium [K] ≥5.1 mEq/L) over a 6-month period. The treatments and their effectiveness, causative factors and associated electrocardiographic (ECG) changes were examined.. There were 154 hyperkalemic episodes, 32 with K ≥6.5 mEq/L and 122 with K<6.5 mEq/L. Overall, 97% received treatment for an average K of 5.9 mEq/L. Sodium polystyrene sulfonate (SPS) was included in 95% of the regimens. Incremental doses of SPS monotherapy yielded potassium reductions between 0.7 and 1.1 mEq/L, and inadequate responses (K <0.5 mEq/L) were less frequent with higher doses. There were no differences in the effectiveness of SPS among dialysis-dependent, chronic kidney disease, or nonchronic kidney disease patients. Greater reductions in potassium were observed using a combination of treatments. ECGs were performed in 44% of patients, and 50% showed no ECG changes despite K being ≥6.5 mEq/L. The most common abnormality, peaked T waves, was associated with a higher frequency of calcium administration but not with the number of K+-lowering therapies.. Almost all the patients were treated for hyperkalemia. Oral SPS monotherapy was the predominant treatment with the best response at the highest dose. Some combination therapies had greater K reductions but were used infrequently. An ECG was obtained in about 50% of the cases, but two thirds showed no K-related changes. Reduced kidney function was associated with 70% of hyperkalemic episodes. Angiotensin-converting enzyme inhibitors and trimethoprim were the most commonly implicated medications.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Albuterol; Calcium; Cation Exchange Resins; Dose-Response Relationship, Drug; Female; Humans; Hyperkalemia; Insulin; Kidney Diseases; Male; Middle Aged; Polystyrenes; Renal Dialysis; Sodium Bicarbonate; Young Adult

Severe hyperkalemia (>7 mmol/L) is a medical emergency because of possible fatal arrhythmias. We here report the case of a 58-year-old woman surviving extreme hyperkalemia (>10 mmol/L). The patient with a history of congestive heart failure, a DDD pacemaker and mild chronic renal insufficiency was admitted with progressive weakness and sudden onset of hypotension and bradycardia in the absence of any pacemaker action. Laboratory tests revealed an extreme serum potassium level of 10.1 mmol/L, with a slightly elevated serum creatinine of 149 μmol/L. Treatment with norepinephrine, sodium bicarbonate, and insulin improved both the hemodynamic situation and the serum potassium with subsequent regaining pacemaker actions even before additional hemodialysis normalized the potassium level. A thorough investigation demonstrated that several mechanisms contributed to the extreme potassium level: urinalysis and a low transtubular potassium gradient in the presence of metabolic acidosis with normal anion gap pointed to preexisting interstitial nephritis, with renal tubular acidosis type IV as the predisposing factor, whereas several drugs and acute impairment of renal function contributed to the dangerous situation. Despite the odds for fatal outcome, the patient recovered completely, and long-term management was initiated to prevent recurrent hyperkalemia.

Topics: Acidosis; Drug Therapy, Combination; Electrocardiography; Emergency Service, Hospital; Female; Humans; Hyperkalemia; Insulin; Middle Aged; Norepinephrine; Potassium; Renal Dialysis; Sodium Bicarbonate; Treatment Outcome

Recent studies evaluated the prevalence of hyperkalemia and related risk factors in patients with CKD of various stages, but there is limited relevant information in predialysis patients. This study aimed to examine the prevalence and factors associated with hyperkalemia in the structured environment of a low-clearance clinic.. In a cross-sectional fashion over a prespecified period of 4 months, information on serum potassium and relevant laboratory variables, comorbidities, medications, and dietician input in patients with advanced CKD under follow-up in the low-clearance clinic of our department was recorded. Univariate and multiple logistic regression analyses were used to identify factors associated with serum potassium ≥ 5.5 meq/L.. The study population consisted of 238 patients aged 66.2 ± 4.2 years with estimated GFR of 14.5 ± 4.8 ml/min per 1.73 m(2). The prevalence of hyperkalemia. defined as potassium > 5.0, ≥ 5.5, and ≥ 6.0 meq/L., was at 54.2%, 31.5%, and 8.4%, respectively. In univariate comparisons, patients with potassium ≥ 5.5 meq/L had significantly higher urea and lower estimated GFR and serum bicarbonate; also, they were more often using sodium bicarbonate and had received potassium education and attempts for dietary potassium lowering. Use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was not associated with hyperkalemia. In multivariate analyses, estimated GFR<15 ml/min per 1.73 m(2) and sodium bicarbonate use were independently associated with hyperkalemia.. The prevalence of hyperkalemia in predialysis patients with CKD is high. Even at this range of renal function, low estimated GFR seems to be the most important factor associated with hyperkalemia among the wide range of demographic, clinical, and laboratory characteristics studied.

Topics: Aged; Aged, 80 and over; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Biomarkers; Chi-Square Distribution; Cross-Sectional Studies; Female; Glomerular Filtration Rate; Humans; Hyperkalemia; Kidney; Logistic Models; London; Male; Middle Aged; Multivariate Analysis; Potassium; Potassium, Dietary; Prevalence; Renal Insufficiency, Chronic; Risk Assessment; Risk Factors; Sodium Bicarbonate; Time Factors

Topics: Acute Kidney Injury; Aged; Bradycardia; Calcium Gluconate; Combined Modality Therapy; Electrocardiography; Emergency Service, Hospital; Follow-Up Studies; Humans; Hyperkalemia; Male; Renal Dialysis; Risk Assessment; Severity of Illness Index; Sodium Bicarbonate; Treatment Outcome

Pseudohypoaldosteronism type 1 is a rare disorder characterized by renal resistance to aldosterone which may present with a salt wasting crisis in infancy. We report a neonate with hyponatremia, severe dehydration and refractory life threatening hyperkalemia who was treated with dietary sodium chloride supplementation, potassium binding resins and fluid replacement therapy which proved to be lifesaving.

Topics: Anti-Inflammatory Agents; Diagnosis, Differential; Fludrocortisone; Fluid Therapy; Humans; Hyperkalemia; Infant, Newborn; Male; Polystyrenes; Pseudohypoaldosteronism; Sodium Bicarbonate; Sodium Chloride

Topics: Aged, 80 and over; Calcium Gluconate; Electrocardiography; Emergency Treatment; Female; Humans; Hyperkalemia; Sodium Bicarbonate

Hyperkalemia generally is attributable to cell shifts or abnormal renal potassium excretion. Cell shifts account for transient increases in serum potassium levels, whereas sustained hyperkalemia generally is caused by decreased renal potassium excretion. Impaired renal potassium excretion can be caused by a primary decrease in distal sodium delivery, a primary decrease in mineralocorticoid level or activity, or abnormal cortical collecting duct function. Excessive potassium intake is an infrequent cause of hyperkalemia by itself, but can worsen the severity of hyperkalemia when renal excretion is impaired. Before concluding that a cell shift or renal defect in potassium excretion is present, pseudohyperkalemia should be excluded.

Topics: Adult; Aldosterone; Chronic Disease; Diabetes Mellitus, Type 1; Diabetic Ketoacidosis; Glomerular Filtration Rate; Humans; Hyperkalemia; Kidney; Kidney Tubules; Liddle Syndrome; Male; Potassium, Dietary; Renin-Angiotensin System; Sodium Bicarbonate

Topics: Adrenergic beta-2 Receptor Agonists; Albuterol; Anti-Arrhythmia Agents; Anticonvulsants; Antihypertensive Agents; Antiparkinson Agents; Antipsychotic Agents; Anxiety Disorders; Atropine; Bradycardia; Calcium Chloride; Diabetes Mellitus; Diagnosis, Differential; Drug Therapy, Combination; Humans; Hyperkalemia; Hypertension; Hypoglycemic Agents; Hypolipidemic Agents; Male; Middle Aged; Muscle Weakness; Polypharmacy; Renal Dialysis; Renal Insufficiency; Sodium Bicarbonate; Sodium Chloride

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Electrocardiography; Enalapril; Humans; Hyperkalemia; Hypertension; Kidney Failure, Chronic; Male; Potassium; Renal Dialysis; Sodium Bicarbonate; Sympathomimetics

Topics: Adrenergic beta-Agonists; Anti-Inflammatory Agents; Calcium Gluconate; Drug Therapy, Combination; Female; Follow-Up Studies; Humans; Hydrocortisone; Hyperkalemia; Hypoaldosteronism; Potassium; Sodium Bicarbonate

Topics: Evidence-Based Medicine; Glucose; Humans; Hyperkalemia; Hypoglycemia; Insulin; Intensive Care Units; Sodium Bicarbonate

A 59-year-old man was referred to the hospital for psychiatric reasons. To control hypertension and chronic heart failure he had been treated with 5 mg ramipril and 12.5 mg hydrochlorothiazide. In addition, he received 25 mg spironolactone. A prostate disease was diagnosed two months ago.. Laboratory analysis revealed a severe hyperkalemia (9.3 mmol/l) as well as an increase in creatinine (24.3 mg/dl) and urea nitrogen (349.0 mg/dl). The ECG showed a bradycardia with increased T-wave amplitudes. Abdominal sonography revealed a full urinary bladder.. Administration of terbutaline, sodium bicarbonate, and glucoseinfusion lowered potassium level to 6.3 mmol/l before hemodialysis was started. Hyperplasia of the prostate gland was found to be the reason for acute renal failure. Dialysis treatment was only temporarily necessary; afterwards, the patient was transferred to the urology department for subsequent therapy.. Hyperkalemia is a life-threatening emergency that requires immediate therapy. Conservative treatment allows to partially correct water-electrolyte imbalance until hemodialysis can be performed. Hyperkalemia often results from the administration of combination therapy with ACE-inhibitors/AT (1)-antaganonists and antikaliuretic diuretics (spironolactone) in renal failure.

Topics: Acute Kidney Injury; Adrenergic beta-Agonists; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Bradycardia; Diuretics; Drug Therapy, Combination; Electrocardiography; Emergencies; Glucose; Heart Failure; Humans; Hydrochlorothiazide; Hyperkalemia; Hypertension; Male; Mental Disorders; Middle Aged; Prostatic Hyperplasia; Ramipril; Renal Dialysis; Sodium Bicarbonate; Terbutaline

Topics: Aged; Aged, 80 and over; Bradycardia; Drug Therapy, Combination; Electrocardiography; Female; Follow-Up Studies; Furosemide; Humans; Hyperkalemia; Risk Assessment; Severity of Illness Index; Sodium Bicarbonate; Treatment Outcome

Topics: Aged; Aged, 80 and over; Cardiotonic Agents; Follow-Up Studies; Hemodiafiltration; Humans; Hyperkalemia; Isoproterenol; Male; Potassium; Quadriplegia; Sodium Bicarbonate; Time Factors

Topics: Alum Compounds; Calcium Sulfate; Causality; Diagnosis, Differential; Electrolytes; Female; Humans; Hyperkalemia; Hypokalemia; Kidney Failure, Chronic; Middle Aged; Pica; Renal Dialysis; Sodium Bicarbonate; Starch

To determine whether alkalinization with sodium bicarbonate (NaHCO3) in near-lethal hyperkalemia either lowers potassium (K) rapidly or shortens duration of cardiac conduction disturbances.. A controlled canine laboratory investigation of 3 treatments for severe hyperkalemia. Conditioned dogs (n = 8; 17-30 kg) received, in random order, 2 mmol/kg of each of 3 treatments (matched in sodium and water) in separate experiments > or = 1 week apart: 1.05% NaHCO3 over 60 minutes (infusion therapy); 8.4% NaHCO3 over 5 minutes, then 14 mL/kg sterile water over 55 minutes (bolus therapy); 8.4% NaCl over 5 minutes, then 14 mL/kg sterile water over 55 minutes (saline therapy). Prior to administering one of the above therapies, the animals were anesthetized with 0.5-2.5% isoflurane and ventilated to maintain a normal PCO2. After 30 minutes of equilibration, 2 mmol/kg/hr (loading dose) of a 2-mmol/mL KCl solution was given until idioventricular or relative junctional bradycardic dysrhythmias were sustained for 15 minutes. Then KCl was decreased to 1 mmol/kg/hr (maintenance dose) for 2 hours and 45 minutes. Treatment was begun after 45 minutes of maintenance KCl infusion.. The pretreatment K level (all studies) was 9.06 +/- 0.82 mmol/L (mean +/- SD). Although the mean K level decreased more after saline therapy than after bolus therapy at every time, differences were neither statistically significant nor clinically important during the first 30 minutes. The means of the differences in decreases (saline minus bolus) were small, 0.26 (95% CI, -0.48 to 1.00) at 15 minutes, 0.16 (95% CI, -0.67 to 0.98) at 30 minutes. Dysrhythmia duration was shorter with bolus therapy than for saline therapy in only 1 of 5 dogs (p = 0.38).. Hypertonic saline bolus lowered plasma K as effectively as NaHCO3 bolus in this animal model within the first 30 minutes. Clinically meaningful decreases due to alkalinization alone within 30 minutes are unlikely.

Topics: Animals; Disease Models, Animal; Dogs; Hyperkalemia; Osmolar Concentration; Sodium Bicarbonate

This study was aimed to evaluate the efficacy of combination therapy of bicarbonate and salbutamol for hyperkalemia in 9 hemodialysis patients. Simultaneous administration of 8.4% sodium bicarbonate (i.v., 2 mEq/kg) for 1/2 hour and salbutamol (15 mg) in nebulized form for 10 min was compared with treatment modality of either bicarbonate or salbutamol alone. Infusion of sodium bicarbonate induced a significant rise in plasma bicarbonate from 17.3 +/- 3.2 to 22.1 +/- 2.4 mEq/L (p < 0.01), but was ineffective in lowering plasma potassium (-0.13 +/- 0.06 mEq/L). As expected, salbutamol significantly lowered plasma potassium (-0.57 +/0 0.03 mEq/L, p < 0.02 vs. basal value) in all except 2 patients. The combined regimen of bicarbonate and salbutamol to a total 9 patients including 2 patients without hypokalemic effect to salbutamol alone revealed a substantially greater fall in plasma potassium (-0.96 +/- 0.08 mEq/L, p = 0.000 vs. either drug alone) accompanied with significant increase in plasma bicarbonate and blood pH. Treatment with salbutamol or the combined regimen produced slight increases in heart rate but not in blood pressure. It is concluded that the combined regimen of bicarbonate and beta(2)-adrenergic agonist (salbutamol) could be recommended as an efficient alternative for severe hyperkalemia in uremic patients, and is suggested that the enhanced transcellular hypokalemic effects of salbutamol in this combined regimen with bicarbonate would be related to the activation of Na-K pump with acute correction of underlying metabolic acidosis.

Topics: Adrenergic beta-Agonists; Adult; Albuterol; Blood Pressure; Drug Therapy, Combination; Female; Heart Rate; Humans; Hydrogen-Ion Concentration; Hyperkalemia; Kidney Failure, Chronic; Male; Middle Aged; Potassium; Sodium Bicarbonate

To describe changes in blood constituents of horses after oral and i.v. administration of sodium bicarbonate (NaHCO3), and to determine whether the changes are dose dependent.. 6 adult Standardbred mares.. 3 oral doses (1,500, 1,000, and 250 mg/kg of body weight) or 1 intravenous dose (250 mg/kg, 5% solution) of NaHCO3 in 3 L of water, or water (3 L orally), were given to the mares; then changes in blood constituents were measured. Access to food and water was denied during the experiment. Blood samples were collected immediately before treatment and at hourly intervals for 12 hours after treatment, and were analyzed for blood gas tensions; serum osmolality; serum sodium, potassium, chloride, and creatinine concentrations; PCV; and total solids concentration in plasma.. All NaHCO3 treatments induced significant (P < 0.05) metabolic alkalosis, hypernatremia, hypokalemia, and hyperosmolality for at least 8 hours. In mares given the 1,500- and 1,000-mg doses of NaHCO3 orally, hypercapnia persisted for at least 12 hours, whereas hypercapnia lasted 2 hours in mares given the 250-mg dose orally or i.v. (P < 0.05). A tendency for reduction in PCV, proteins in plasma concentration, and serum concentration of chloride was observed 1 hour after i.v. administered doses of NaHCO3.. Oral or i.v. administration of NaHCO3 (> or = 250 mg/kg) to resting horses without ad libitum access to water induces significant and persistent acid-base and electrolyte changes.

Topics: Acid-Base Equilibrium; Administration, Oral; Alkalosis; Animals; Blood Gas Analysis; Blood Proteins; Chlorides; Creatinine; Dose-Response Relationship, Drug; Female; Horses; Hydrogen-Ion Concentration; Hyperkalemia; Hypernatremia; Injections, Intravenous; Osmolar Concentration; Potassium; Sodium; Sodium Bicarbonate; Time Factors

Application of sodium bicarbonate is still an option when resuscitation efforts remain unsuccessful. Despite this, there are no recommendations on how long resuscitation should be performed after administration of this drug. Here we describe a case in which prehospital resuscitation efforts were terminated about 35 min after cardiac arrest. Seven minutes after all efforts had been discontinued, spontaneous sinus rhythm appeared from a zero-line ECG, giving normal hemodynamic values. The underlying reason might be unexpected and unrecognized hyperkalemia, which was diminished by administration of sodium bicarbonate, even under the conditions of cardiocirculatory arrest.

Topics: Cardiopulmonary Resuscitation; Electrocardiography; Heart Arrest; Hemodynamics; Humans; Hyperkalemia; Male; Middle Aged; Myocardial Contraction; Sodium Bicarbonate; Time Factors

Topics: Adult; Arrhythmias, Cardiac; Bicarbonates; Electrocardiography; Female; Humans; Hyperkalemia; Male; Middle Aged; Sodium; Sodium Bicarbonate

To examine whether an acute increase in plasma potassium concentration ([K]p) may inhibit proximal tubular transport, clearance studies were performed in seven anaesthetized, volume expanded dogs treated with amiloride (1 mg kg-1 body wt) to block tubular potassium secretion, and with bumetanide (30 micrograms kg-1 body wt) to inhibit NaCl reabsorption in Henle's loop. As [K]p was raised in steps from 2.6 +/- 0.2 to 7.9 +/- 0.2 mM, bicarbonate, chloride, and sodium reabsorption decreased by 232 +/- 56, 520 +/- 59 and 958 +/- 112 mumol min-1, respectively, at constant glomerular filtration rate (GFR). On average, the molar ratio between the inhibitory effects on bicarbonate and chloride reabsorption were 1:2.2-2.4. Reabsorption was calculated at GFR 100 ml min-1: (reabsorption 100/GFR (mmol min-1). It was inversely correlated to ln [K]p with r = -0.82 for bicarbonate and with r = -0.89 for chloride. Fractional potassium reabsorption remained constant at 0.31 +/- 0.03. Administration of acetazolamide (100 mg kg-1 body wt) in eight dogs at [K]p 8 mM reduced fractional reabsorption of bicarbonate, chloride and sodium as much as in previous studies on normokalaemic dogs. We conclude that acute elevation of [K]p inhibits NaHCO3 transport and passive proximal tubular NaCl reabsorption. This inhibition is not related to changes in potassium secretion and carbonic anhydrase activity, but may be secondary to depolarization of the basolateral membrane.

Topics: Absorption; Acetazolamide; Amiloride; Animals; Bicarbonates; Biological Transport; Bumetanide; Dogs; Dose-Response Relationship, Drug; Female; Glomerular Filtration Rate; Hyperkalemia; Kidney Tubules, Proximal; Male; Metabolic Clearance Rate; Potassium; Sodium; Sodium Bicarbonate; Sodium Chloride

Topics: Bicarbonates; Calcium Gluconate; Education, Medical; Humans; Hyperkalemia; Kidney Failure, Chronic; Nephrology; Renal Dialysis; Sodium; Sodium Bicarbonate; Surveys and Questionnaires; United States

Topics: Bicarbonates; Calcium Gluconate; Humans; Hyperkalemia; Kidney Failure, Chronic; Sodium; Sodium Bicarbonate

Topics: Bicarbonates; Calcium Gluconate; Humans; Hyperkalemia; Hypokalemia; Polystyrenes; Potassium; Sodium; Sodium Bicarbonate

Two newborn infants with ventricular arrhythmias secondary to hyperkalaemia are presented. One child also showed a decreased serum calcium concentration. There is scanty literature concerning the often life threatening cardiac arrhythmias due to hyperkalaemia in the newborn infants. Treatment of the cardiac arrhythmias require intravenous calcium gluconat and sodium bicarbonate infusion beside lowering the serum potassium level in the usual way.

Topics: Bicarbonates; Calcium Gluconate; Female; Humans; Hyperkalemia; Infant, Newborn; Infusions, Intravenous; Male; Sodium; Sodium Bicarbonate; Tachycardia

We prospectively evaluated 30 patients who presented with active systemic lupus erythematosus (SLE) for the presence of tubular abnormalities. All patients fulfilled the American Rheumatology Association criteria for SLE. When appropriate, a renal biopsy was performed. Of the 30 patients studied, 12 had no abnormal tubular study results, whereas 18 patients had some form of defect in the handling of potassium, sodium, or hydrogen ions. Eight patients had distal renal tubular acidosis (dRTA) due to an isolated proton secretory defect. Five had dRTA of the gradient or acid back-leak type. Two had an unresponsive voltage-dependent form of dRTA; one had a responsive voltage-dependent form of dRTA. One individual had hyporeninemic hypoaldosteronism and one had dRTA plus hypoaldosteronism. Clinically, patients with the abnormal tubular study results more often presented with nephritis or nephrotic sediment, peripheral edema, or anemia. Renal biopsies failed to demonstrate any difference in glomerular histologic findings and calculated activity, chronicity, or interstitial indexes. We conclude that SLE may be associated with a variety of tubular defects.

Topics: Acidosis, Renal Tubular; Adult; Ammonium Chloride; Bicarbonates; Female; Humans; Hyperkalemia; Kidney; Kidney Tubules; Lupus Nephritis; Male; Prospective Studies; Sodium; Sodium Bicarbonate; Sulfates

Topics: Acidosis, Renal Tubular; Aged; Bicarbonates; Calcium Gluconate; Female; Humans; Hyperkalemia; Injections, Intravenous; Insulin; Ion Exchange Resins; Quadriplegia; Sodium; Sodium Bicarbonate; Spironolactone

We observed a 23-year-old man with pronounced hyperkalemia (max. 6.8 mmol/l) and hyponatremia (min. 112 mmol/l), which had been existent for 3 years without complaint except a transitory psychorganic syndrome due to hyponatremia. Physical examination showed no abnormality except hypotension (blood pressure 100/70 mmHg). Renal function tests were normal. Fractional clearance of sodium was significantly increased (0.8%), whereas that of potassium was decreased (2.4%). Plasma renin activity was tripled and rose after furosemide. Plasma aldosterone was lowered and showed no rise after furosemide. Suppression of plasma renin and aldosterone by saline infusion was normal. Pressor dose of angiotensin II was increased (17,9 ng AT II/kg/min). Urinary excretion of aldosterone and its conjugates was below normal, and aldosterone precursors were within normal range. The findings were interpreted as selective primary hypoaldosteronism caused by corticosterone methyl oxidase defect type II. However, neither fludrocortisone (0.5 mg/day) nor sodium chloride (200 mmol/day) led to a normalization of sodium and potassium in plasma. Additional pseudohypoaldosteronism was thus assumed. Aldosterone infusion (3 mg in 1 h) decreased renal excretion of sodium; potassium excretion failed, however, to increase in contrast to its pattern in normal man. These findings resemble additional pseudohypo-aldosteronism of type II. After 8 weeks' application of additional 80 mmol sodium (as sodium bicarbonate) plasma sodium and potassium showed normal values under combined treatment with fludrocortisone (0.1 mg/day) and sodium bicarbonate (80 mmol/day). It is to be assumed that the patient suffers from a reduced aldosterone biosynthesis in the presence of an additional transitory secondary pseudohypoaldosteronism.

Topics: Adult; Aldosterone; Angiotensin II; Bicarbonates; Fludrocortisone; Humans; Hyperkalemia; Hyponatremia; Male; Potassium; Renin; Sodium; Sodium Bicarbonate; Sodium Chloride; Water-Electrolyte Balance

Topics: Bicarbonates; Calcium; Calcium Channel Blockers; Cation Exchange Resins; Diuretics; Humans; Hypercalcemia; Hyperkalemia; Insulin; Polystyrenes; Sodium Bicarbonate; Uremia

Topics: Acidosis; Bicarbonates; Humans; Hyperkalemia; Potassium; Sodium Bicarbonate; Uremia