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Pediatric Hyperkalemia Medication

  • Author: Michael J Verive, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
Updated: Jan 08, 2016

Medication Summary

Treatment for severe hyperkalemia consists of 3 steps: (1) immediate stabilization of the myocardial cell membrane, (2) rapidly shifting potassium intracellularly, and (3) enhancing total body potassium elimination (see Medical Care).

In addition, all sources of exogenous potassium should be immediately discontinued; including intravenous (IV) and oral (PO) potassium supplementation, total parenteral nutrition, and any blood product transfusion. Drugs associated with hyperkalemia should also be discontinued.

Albuterol and other beta-adrenergic agents induce the intracellular movement of potassium via the stimulation of the sodium/potassium–adenosine triphosphate (Na+/K+ -ATP) pump. Studies have shown that IV salbutamol (not available in the United States) is highly effective in lowering serum potassium levels. Some studies in adults and children using nebulized albuterol indicate that this method of therapy is effective in lowering serum potassium levels. However, peak response is unclear; therefore, it has not been established as the first line of therapy in severe hyperkalemia.


Myocardium stabilizers

Class Summary

Calcium does not lower serum potassium levels. It is primarily used to protect the myocardium from the deleterious effects of hyperkalemia (ie, arrhythmias) by antagonizing the membrane actions of potassium.

Calcium chloride


IV calcium is indicated in all cases of severe hyperkalemia (ie, >7 mEq/L), especially when accompanied by ECG changes. Calcium chloride contains about 3 times more elemental calcium than an equal volume of calcium gluconate. Therefore, when hyperkalemia is accompanied by hemodynamic compromise, calcium chloride is preferred over calcium gluconate.

Administration of calcium should be accompanied by the use of other therapies that actually help lower the K+ serum levels.

Other calcium salts (eg, glubionate, gluceptate) have even less elemental calcium than calcium gluconate and are generally not recommended for therapy of hyperkalemia. Calcium chloride 1 g = 270 mg (13.5 mEq) of elemental calcium.

Calcium gluconate 1 g = 90 mg (4.5 mEq) of elemental calcium.


Intracellular transporters

Class Summary

Regular insulin and glucose cause a transcellular shift of potassium into muscle cells, thereby temporarily lowering K+ serum levels.

Insulin and dextrose, IV


Regular insulin presence results in intracellular movement of glucose, followed by K+ entry into muscle cells. Although effect is almost immediate, it is temporary, and, therefore, should be followed by therapy that actually enhances potassium clearance (eg, sodium polystyrene sulfonate).


Alkalinizing agents

Class Summary

Sodium bicarbonate IV is used as a buffer that breaks down to water and carbon dioxide after binding free hydrogen ions.

Sodium bicarbonate


IV infusion helps shift K+ into cells, further lowering serum K+ levels. Can be considered in treatment of hyperkalemia even in absence of metabolic acidosis. Also increases sodium delivery to the kidney, which assists in potassium excretion.


Exchange resins

Class Summary

Sodium polystyrene sulfonate is an exchange resin that can be used to treat mild-to-moderate hyperkalemia. Each mEq of potassium is exchanged for 1 mEq of sodium.

Sodium polystyrene sulfonate (Kayexalate)


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

Do not use as a first-line therapy for severe life-threatening hyperkalemia. Use in second stage of therapy to reduce total body potassium.

Contributor Information and Disclosures

Michael J Verive, MD, FAAP Pediatrician, UP Health System Portage

Michael J Verive, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, Society for Pediatric Sedation

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society

Disclosure: Nothing to disclose.

Additional Contributors

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

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Peaked T waves.
Sinusoidal wave.
Hyperkalemia diagnosis and treatment flow chart.
Table. Select 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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