• Potassium is largely an intracellular electrolyte
  • Intracellular potassium is regulated through the Na+/K+ ATPase channel
  • Normal serum K+ levels: 3.5 – 5.0 mEq/L
  • Consider repeating lab draw: False hyperkalemic readings may results from drawing from an IV with a potassium-rich fluid running through it. Also, prolonged tourniquet constriction of arm during blood draw can cause localized cell lysis and false readings of hyperkalemia


  • High intake
    • Lactated Ringer’s
    • Penicillin G
    • Total parenteral nutrition (TPN)
  • Low output (90% of serum K+ is excreted through the kidney 1)
    • Acute Kidney Injury (AKI)
    • Type 4 Renal Tubular Acidosis (Hypoaldosteronism)
    • Medications (Most of these share the end effect of decreasing the level of aldosterone in the body)
      • ACE Inhibitors (ACEI): Lisinopril, captopril, etc.
      • Angiotensin-Receptor Blockers (ARBs): Losartan, valsartan, etc.
      • Aldosterone-Receptor Antagonists: Spironolactone, eplerenone
      • Epithelial Na+ channel (ENaC) inhibitors: Amiloride, triamterene
      • NSAIDs
      • Ketoconazole (inhibits aldosterone synthase)
  • K+ shifting from intracellular to extracellular
    • Acidemia: Stimulates H+/K+ exchange channels, shifting H+ inside the cell and K+ out of the cell
    • Hypertonicity: Causes water to flow out of cell, potassium moves with it
    • Cell Lysis
      • Tumor Lysis Syndrome
      • Rhabdomyolysis
      • Trauma
      • Hemolysis

EKG changes

  • 1st: “Peaked” T-waves
  • 2nd: Prolonged PR interval
  • 3rd: Loss of P-waves
  • 4th: Prolonged QRS interval
  • 5th: Sinusoidal waves
  • 6th: Ventricular arrhythmia


  • Stabilize the cardiac membrane
    • Calcium gluconate
      • Indications: Conduction abnormalities on EKG or significantly elevated potassium level (generally > 6.5 mEq/L)
      • Physiology: The Nernst equation tells us that in hyperkalemia, the resting membrane potential is shifted to a less negative value. Therefore, a lower stimulation is necessary to generate an action potential. However, after repeated depolarizations, sodium channels in the membrane become inactivated. This leads to a decreased ability of the cardiac muscle to generate action potentials (2). Administration of calcium shifts the threshold potential of the membrane to a less negative value, so that the difference between the resting membrane potential and the threshold potential remains ~15 mV (3)
      • Effect lasts ~30 minutes, so repeated administration is necessary if still indicated
  • Decrease serum potassium levels
    • Quick, temporary
      • IV Regular Insulin
        • Stimulates Na+/K+ ATPase
        • Give D50W at the same time to avoid hypoglycemia
      • IV Sodium Bicarbonate
        • Increases serum pH, causing cell membrane H+/K+ exchange channels to activate, shifting H+ outside the cell and K+ into the cell
      • β-2 agonist (e.g. albuterol)
        • Stimulates Na+/K+ ATPase
    • Slow, permanent
      • Loop diuretics (e.g. furosemide)
        • Increase renal excretion of potassium
      • Sodium polystyrene
        • Increases GI excretion of potassium (but, as above, ~90% of potassium is excreted through kidneys)
  • Dialysis
    • Indicated if:
      • Symptomatic (weakness/paralysis)
      • Conduction abnormalities on EKG
      • Hyperkalemia refractory to above therapies
      • Severe renal dysfunction
      • Significantly elevated potassium level (generally > 6.5 mEq/L)


  1. Nohara‐Shitama, Y., Yume Nohara‐Shitama Division of Cardio‐Vascular Medicine, Adachi, H., Hisashi Adachi Division of Cardio‐Vascular Medicine, Enomoto, M., Mika Enomoto Division of Cardio‐Vascular Medicine, . . . Adachi, *. (2018, January 04). Twenty‐four‐Hour Urinary Potassium Excretion, But Not Sodium Excretion, Is Associated With All‐Cause Mortality in a General Population. Retrieved January 12, 2021, from https://www.ahajournals.org/doi/full/10.1161/jaha.117.007369
  2. RM, B., & MN, L. (1981). Cardiovascular Physiology, 4th edition. St. Louis, MO: Mosby.
  3. Parham, W., Mehdirad, A., Biermann, K., & Fredman, C. (2006). Hyperkalemia revisited. Retrieved January 12, 2021, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/

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