Hyperkalemia Medication

  • Author: Eleanor Lederer, MD; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Dec 16, 2011
 

Medication Summary

The goals of pharmacotherapy are to reduce potassium levels and morbidity and to prevent complications.

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Beta-adrenergic agonists

Class Summary

Through an activation of cyclic adenosine monophosphate (AMP), these agonists stimulate the adenosine triphosphatase (ATPase) pump, thereby shifting potassium into the intracellular compartment.

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Isoproterenol (Dey-Dose, Isuprel, Arm-a-Med)

 

Has beta1-adrenergic and beta2-adrenergic receptor activity.

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Albuterol (Proventil, Ventolin)

 

Adrenergic agonist that increases plasma insulin concentrations. Increase in insulin may shift potassium into intracellular space.

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Calcium salts

Class Summary

Calcium antagonizes cardiotoxicity of hyperkalemia by stabilizing cardiac cell membrane against undesirable depolarization. Has no effect on serum level of potassium. Onset of effect is rapid, within 15 min, but relatively short lived.

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Calcium gluconate (Kalcinate)

 

Moderates nerve and muscle performance and facilitates normal cardiac function.

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Calcium chloride

 

Prevents deleterious effects caused by severe hyperkalemia as measured by ECG, pending correction of increased potassium in extracellular fluid. Generally, second choice to calcium gluconate due to irritating effects when administered parenterally.

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Hormones

Class Summary

Insulin stimulates cellular uptake of potassium, lowering serum potassium level.

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Insulin regular human (Novolin, Humulin)

 

Stimulates cellular uptake of potassium within 20-30 min. Administer glucose along with insulin to prevent hypoglycemia. Monitor blood sugar levels frequently.

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Diuretics

Class Summary

Loop diuretics markedly enhance renal potassium excretion, consequently lowering serum levels. Parenterally administered drug has a more rapid onset of action and is preferable in emergent situations. Simultaneous administration of saline can prevent severe volume depletion.

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Furosemide (Lasix)

 

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in ascending loop of Henle and distal renal tubule. Individualize dose to patient. Depending on the response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate with increments of 1 mg/kg per dose until a satisfactory effect is achieved. Oral absorption of furosemide is variable from person to person. If rapid and effective therapy is mandated, then IV route is preferred. Occasionally, a continuous infusion of furosemide, as high as 40 mg/h, is used for severe edema but rarely is required for the treatment of hyperkalemia.

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Bumetanide (Bumex)

 

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in ascending loop of Henle and distal renal tubule. Individualize dose to patient. Start at 1-2 mg IV; titrate to as high as 10 mg/d. Rarely, doses as high as 24 mg/d are used for edema but generally are not required for treatment of hyperkalemia.

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Cation exchange resins

Class Summary

Stimulate the exchange of sodium for potassium in the colon, thus increasing intestinal excretion of potassium.

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Sodium polystyrene sulfonate (Kayexalate)

 

Exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, and decreases total body potassium. Onset of action after oral administration ranges from 2-12 h and is longer when administered rectally.

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Electrolytes

Class Summary

Used to correct metabolic acidosis if acidosis is severe.

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Sodium bicarbonate (Neut)

 

Used only when patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, tricyclic antidepressant overdose, or phenobarbital overdose. Routine use is not recommended.

To estimate the dose that should be administered may use the following formula: HCO3- (mEq) = 0.5 X weight in kg X (24 - serum HCO3- in mEq/L)

This formula has many limitations; however, the practitioner can determine roughly the amount of bicarbonate required and subsequently titrate against the pH and anion gap.

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Contributor Information and Disclosures
Author

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

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Coauthor(s)

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.

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

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

Disclosure: Nothing to disclose.

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.

Specialty Editor Board

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.

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 Federation for Medical Research, American Heart Association, American Society of Nephrology, American Society of Transplantation, American Thoracic Society, International Society of Nephrology, and Royal College of Physicians

Disclosure: Nothing to disclose.

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Renal Ventures Ownership interest Other

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, 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, and International Society of Nephrology

Disclosure: Nothing to disclose.

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Peaked T waves on an electrocardiogram, as seen in hyperkalemia.
Widened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L.
 
 
 
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