Mnemonic Monday: Causes and Management of Hyperkalemia: C BIG K DI

mnemonicsBy Michael Spinner

Hyperkalemia is one of the most important and frequently encountered electrolyte abnormalities. Today’s post is intended to serve as a review of the most common causes of hyperkalemia and the approach to management of this electrolyte abnormality, both acutely and chronically.

First, recall a few key concepts from normal potassium homeostasis:

  • Potassium enters the body via oral intake or intravenous infusion
  • Potassium is mainly stored within cells as the major intracellular cation; this is maintained by the Na-K-ATPase pump
  • Potassium is excreted by the kidneys, and mineralocorticoids like aldosterone promote potassium excretion

Hyperkalemia may thus result from any of the following causes:

  • Excessive potassium intake (usually iatrogenic)
  • Increased potassium release from cells (rhabdomyolysis, burns, hemolysis after blood transfusion, tumor lysis syndrome, extracellular shifts ? acidosis, insulin deficiency/DKA, beta blockers)
  • Decreased potassium excretion (acute or chronic renal failure, potassium-sparing diuretics like spironolactone or amiloride, aldosterone deficiency, ACE inhibitors, angiotensin receptor blockers)

Another common cause of an elevated serum potassium is “pseudohyperkalemia,” a laboratory artifact resulting from a hemolyzed blood sample. A repeat potassium level should be checked if psuedohyperkalemia is suspected.

The most dangerous manifestations of hyperkalemia are cardiac conduction abnormalities and arrhythmias. Thus, the first step in the evaluation of hyperkalemia should be obtaining an EKG. Hyperkalemia may result in a progression of EKG changes including peaked T waves and QT interval shortening, PR and QRS interval prolongation, and finally a sine wave appearance. After obtaining an EKG, the approach to hyperkalemia management can be remembered with the mnemonic “C BIG K DI” (i.e. if you see a big K, the patient could die!):

CCalcium gluconate (stabilizes cardiac membrane)
BBeta-2 agonists (nebulized albuterol) or Bicarbonate (both shift K into cells)
IGInsulin + Glucose (insulin shifts K into cells + glucose to avoid hypoglycemia)
KKayexalate (binds K in gut, excreted in feces lowering total body K stores)
DIDIuretics (lasix) or DIalysis (if refractory to all other treatment options)

This is one of my favorite mnemonics! I hope it will serve you well on the wards!

Further reading:
UpToDate – Causes and evaluation of hyperkalemia in adults
UpToDate – Treatment and prevention of hyperkalemia in adults


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