Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android. Learn more here!


  • Serum potassium levels reflect only 2% of total body potassium.

  • Therapy for hyperkalemia is aimed at halting intake, stabilizing cellular membranes, intracellular translocation, and enhancing elimination.

  • Hypokalemia should be corrected orally, if possible. Extreme caution should be exercised during intravenous replacement to avoid hyperkalemia.


While only 2% of total body potassium is in the extracellular fluid (ECF), potassium is the main cation in intracellular fluid (ICF). Normal potassium concentration in the ECF is 3.5 to 5.5 mEq/L, compared to approximately 160 mEq/L in the ICF. The sodium–potassium ATPase pump in the cell membrane maintains this large concentration gradient.

Potassium homeostasis is managed through the use of both translocation and excretion. The majority of potassium excretion occurs in the kidney. The kidney can adjust urinary potassium excretion from 5 to 1000 mEq/24 h. Approximately 5% of daily potassium intake is lost through the gastrointestinal tract in stool.

As only 50% of a potassium load is excreted in the first 4 to 6 hours, translocation allows the body to maintain stable ECF potassium. In the first hours after ingestion, potassium is translocated into cells, primarily in the liver and muscle. Potassium uptake is regulated by insulin, catecholamines, aldosterone, and acid–base balance.1 Insulin stimulates the sodium–potassium ATPase pump to promote potassium uptake in the liver and muscle. Catecholamines cause an initial rise in serum potassium as it is released from the liver. Subsequently, serum potassium falls as catecholamines promote movement to ICF. Aldosterone acts through both renal and extrarenal mechanisms to reduce serum potassium. Acid–base changes direct potassium shifts. Acidemia promotes movement of potassium to the ECF, whereas alkalosis favors movement of potassium to the ICF.


Hyperkalemia is defined as serum potassium >5.5 mEq/L and can result from increased potassium intake, decreased potassium loss, or from redistribution from the ICF. Increased potassium intake rarely results in an elevation of serum potassium, unless it is iatrogenic or simultaneously associated with decreased excretion. Iatrogenic causes include excessive intravenous administration of potassium, administration of large quantities of cold-stored blood, large doses of the potassium salts of penicillin, or oral intake of potassium-containing salt substitutes. Acute renal failure is the primary cause of decreased excretion. Less commonly, adrenal insufficiency may result in hyperkalemia due to decreased mineralocorticoid activity. Use of potassium-sparing diuretics is also associated with decreased potassium excretion.1

Redistribution of potassium from the ICF to the ECF may occur via cell destruction or translocation from intact cells. In patients with trauma, burns, rhabdomyolysis, massive intravascular coagulopathy, or tumor lysis/necrosis, injured cells release stores of intracellular potassium into the circulation. Hematomas in the newborn and gastrointestinal bleeding may result in large volumes of hemolyzing cells and elevated potassium levels. Potassium can be quickly shifted from the ICF to the ECF in response to metabolic acidosis. The ICF is ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.