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Hyperkalemia Medication

  • Author: Eleanor Lederer, MD, FASN; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Jan 11, 2016
 

Medication Summary

The goals of pharmacotherapy are to reduce potassium levels and morbidity and to prevent complications. Calcium protects the myocardium from the deleterious effects of hyperkalemia. Beta-adrenergic agents, insulin, and loop diuretics stimulate cellular uptake of potassium, lowering the serum potassium level.

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Calcium salts

Class Summary

Calcium antagonizes the cardiotoxicity of hyperkalemia by stabilizing the cardiac cell membrane against undesirable depolarization. Onset of effect is rapid (≤ 15 minutes) but relatively short-lived. These agents are the first-line treatment for severe hyperkalemia (ie, >7 mEq/L), when the electrocardiogram (ECG) shows significant abnormalities (eg, widening of QRS interval, loss of P wave, or cardiac arrhythmias). Calcium usually is not indicated when the ECG shows only peaked T waves.

Calcium has no effect on the serum level of potassium. For that reason, administration of calcium should be accompanied by the use of other therapies that actually help lower serum potassium levels.

Calcium chloride contains about 3 times more elemental calcium than an equal volume of calcium gluconate: 1 g of calcium chloride has 270 mg (13.5 mEq) of elemental calcium, whereas 1 g of calcium gluconate has 90 mg (4.5 mEq). Therefore, when hyperkalemia is accompanied by hemodynamic compromise, calcium chloride is preferred to calcium gluconate. Other calcium salts (eg, glubionate and gluceptate) have even less elemental calcium than calcium gluconate and generally are not recommended for therapy of hyperkalemia.

Calcium gluconate

 

Calcium increases the threshold potential, thus restoring the normal gradient between threshold potential and resting membrane potential, which is abnormally elevated in hyperkalemia. Onset of action is within 5 minutes, and duration of action is about 30-60 minutes. Doses should be titrated with constant monitoring of ECG changes during administration; repeat the dose if ECG changes do not normalize within 3-5 minutes.

Calcium chloride

 

Calcium prevents the deleterious cardiac effects of severe hyperkalemia that may occur before the serum potassium level is corrected. Because of its irritating effects when administered parenterally, calcium chloride is generally considered a second choice, after calcium gluconate.

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Beta-adrenergic agonists

Class Summary

Through activation of cyclic adenosine monophosphate (cAMP), these agonists stimulate the sodium-potassium–adenosine triphosphatase (Na+ -K+ -ATPase) pump, thereby shifting potassium into the intracellular compartment. However, these shifts in potassium occur primarily during exercise rather than at rest.

Albuterol (Proventil, Ventolin, Vospire ER)

 

Albuterol is an adrenergic agonist that has an additive effect with insulin and glucose, which may in turn help shift potassium into the intracellular space. This agent lowers the serum potassium level by 0.5-1.5 mEq/L. It can be very beneficial in patients with renal failure when fluid overload is concern. Onset of action is 30 minutes; duration of action is 4-6 hours for the immediate-release product.

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Antidiabetics, Insulins

Class Summary

Insulin is administered with glucose to facilitate the uptake of glucose into muscle cells, bringing potassium with it, primarily by enhancing the activity of the Na+ -K+ -ATPase pump and thereby temporarily lowering serum potassium levels.

Insulin regular human (Novolin R, Humulin R)

 

Regular insulin stimulates cellular uptake of potassium within 20-30 minutes and lasts for 4-6 hours. The serum potassium concentration typically drops by 0.5-1.2 mEq/L. Administer glucose along with insulin to prevent hypoglycemia. Monitor blood sugar levels frequently. Although the effect is rapid, it is temporary; therefore, insulin therapy should be followed by therapy that actually enhances potassium clearance (eg, sodium polystyrene sulfonate [SPS]).

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Diuretics, Loop

Class Summary

Loop diuretics markedly enhance renal potassium excretion and thus lower serum levels. Parenterally administered drugs have a more rapid onset of action and are preferable in emergency situations. Simultaneous administration of saline can prevent severe volume depletion.

Furosemide (Lasix)

 

Furosemide increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Furosemide has a slow onset of action (frequently 1 hour), and its effect on lowering the potassium level is inconsistent. Large doses may be needed in renal failure.

Individualize the dose to the patient. For the treatment of edema, depending on the response, administer in increments of 20-40 mg, no sooner than 6-8 hours after the previous dose, until the desired diuresis occurs. When treating infants and children, give 1-2 mg/kg every 6-12 hours. If the diuretic response is not satisfactory, furosemide may be titrated in increments of 1 mg/kg (no sooner than 2 hours after the previous dose) until a satisfactory effect is achieved (up to 6 mg/kg).

Oral absorption of furosemide varies from person to person. If the patient requires rapid and effective therapy, the intravenous (IV) route is preferred. Continuous infusion of furosemide (at rates as high as 40 mg/hr) is occasionally used for severe edema but rarely is required for the treatment of hyperkalemia.

Bumetanide (Bumex)

 

Bumetanide increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Individualize the dose to the patient.

For treatment of edema in adults, start at 0.5-1 mg IV or intramuscularly (IM); if the desired response is not achieved, administer a second or third dose at 2-3 hour intervals. Titrate to a maximum dosage of 10 mg/day. Rarely, dosages as high as 20 mg/day are used for edema in patients with renal impairment; however, they generally are not required for treatment of hyperkalemia.

Ethacrynic acid (Edecrin)

 

Ethacrynic acid increases excretion of water by interfering with the chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. For treatment of edema in adults, start at 0.5-1 mg/kg IV. Typically, 1 dose is all that is needed; occasionally, however, a second dose may be given after 2-4 hours. For second doses, a new injection site should be used so as to avoid possible thrombophlebitis. Single IV doses higher than 100 mg are not recommended.

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Potassium Binders

Sodium polystyrene sulfonate (Kayexalate, Klonex, Kalexate, SPS)

 

SPS exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, decreasing the total body potassium level by approximately 0.5-1 mEq/L. Multiple doses are usually necessary.

Onset of action ranges from 2 to 24 hours after oral administration and is even longer after rectal administration. The duration of action is 4-6 hours. Do not use SPS as a first-line therapy for severe life-threatening hyperkalemia; use it in the second stage of therapy.

The US Food and Drug Administration (FDA) notes that SPS has been associated with intestinal necrosis and other serious gastrointestinal (GI) complications and advises against its use in patients who do not have normal bowel function. Concomitant use of sorbitol with sodium polystyrene sulfonate has been implicated in cases of colonic necrosis.[62]

Patiromer (Veltassa)

 

Patiromer sorbitex calcium is a nonabsorbed, cation exchange polymer that contains a calcium-sorbitol counterion. It increases fecal potassium excretion by binding potassium in the lumen of the GI tract. It is indicated for hyperkalemia. It should not be used as an emergency treatment for life-threatening hyperkalemia because of its delayed onset of action.

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Alkalinizing Agents

Class Summary

In patients with severe metabolic acidosis, sodium bicarbonate IV is used as a buffer that breaks down to water and carbon dioxide after binding free hydrogen ions. By increasing the pH, sodium bicarbonate promotes a temporary potassium shift from the extracellular to the intracellular environment. It also enhances the effectiveness of insulin in patients with acidemia. These agents have been successfully used in the treatment of acute overdose of slow-release oral potassium preparations.

The use of sodium bicarbonate can be considered in treatment of hyperkalemia even in the absence of metabolic acidosis, though it is less likely to be effective in this context. This agent also increases sodium delivery to the kidney, which assists in potassium excretion.

Sodium bicarbonate

 

The bicarbonate ion neutralizes hydrogen ions and raises urinary and blood pH. Onset of action occurs within minutes; duration of action is approximately 15-30 minutes. Monitor blood pH to avoid excess alkalosis. Use the 8.4% solution in adults and children and the 4.2% solution in children younger than 2 years. The adult dose for hyperkalemia is 50 mEq IV over 5 minutes. Consider methods of enhancing potassium removal or excretion, as appropriate.

The following formula may be used to estimate the dose that should be administered for metabolic acidosis:

HCO3− (mEq) = 0.5 (L/kg) × weight (kg) × (24 − serum HCO3− [mEq/L])

This formula has many limitations; however, it allows the practitioner to make a rough determination of the amount of bicarbonate required and subsequently to titrate against the pH and anion gap.

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Electrolytes

Class Summary

Magnesium sulfate is used for hyperkalemic patients with cardiac arrhythmias from digitalis toxicity.

Magnesium sulfate

 

Magnesium is a cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. In adults, potassium 60-180 mEq/day, magnesium 10-30 mEq/day, and phosphate 10-40 mmol/day may be necessary for optimum metabolic response. Give IV for acute suppression of torsades de pointes. Repeat doses are dependent on the continuing presence of patellar reflex and adequate respiratory function.

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Contributor Information and Disclosures
Author

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Coauthor(s)

Vibha Nayak, MD Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville School of Medicine

Vibha Nayak, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Zygimantas C Alsauskas, MD Assistant Professor of Medicine, Division of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

Zygimantas C Alsauskas, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Lina Mackelaite, MD Assistant Professor of Medicine, University of Louisville School of Medicine

Lina Mackelaite, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Transplantation, National Kidney Foundation

Disclosure: Nothing to disclose.

Specialty Editor Board

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Acknowledgements

Son Dinh, MD Nephrologist, Southland Renal Medical Group, Inc

Son Dinh, MD is a member of the following medical societies: American Society of Nephrology and National Kidney Foundation

Disclosure: Nothing to disclose.

Anil Kumar Mandal, MD Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School of Medicine

Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Nothing to disclose.

Rosemary Ouseph, MD Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine

Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, and American Society of Transplant Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

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Widened QRS complexes in patient whose serum potassium level was 7.8 mEq/L.
ECG of patient with pretreatment potassium level of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule of calcium chloride. Note narrowing of QRS complexes and reduction of T waves.
Hyperkalemia diagnosis and treatment flow chart.
Widened QRS complexes in hyperkalemia.
Table. Selected Factors Affecting Plasma Potassium
Factor Effect on Plasma K+ Mechanism
Aldosterone Decrease Increases sodium resorption, and increases K+ excretion
Insulin Decrease Stimulates K+ entry into cells by increasing sodium efflux (energy-dependent process)
Beta-adrenergic agents Decrease Increases skeletal muscle uptake of K+
Alpha-adrenergic agents Increase Impairs cellular K+ uptake
Acidosis (decreased pH) Increase Impairs cellular K+ uptake
Alkalosis (increased pH) Decrease Enhances cellular K+ uptake
Cell damage Increase Intracellular K+ release
Succinylcholine Increase Cell membrane depolarization
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