Calcium and Hyperkalemia

Calcium Chloride/Gluconate are used during Hyperkalemia induced ECG changes to reduce Serum Potassium.

The answer is: False!

The majority of Potassium in our body is found intracellular. Only a very small percentage (about 2%) is found extracellular, ranging between 3.5- 5.5 mEq/L.

As extracellular Potassium levels increase, the action potential threshold decreases, for example, instead of -90mV, now its -80mV. Remember, the Sodium-Potassium ATPase pump controls these ions, so as Hyperkalemia worsens, the amount of Sodium influx also decreases. All of these factors lead to decreased ventricular conduction, causing  shorter QT Intervals, ST-T wave abnormalities and wide QRS complexes on the ECG.

You will not always get the classic “Peaked T” waves or bizarre QRS complex morphologies, but this does not mean that there is no Hyperkalemia, or there is no life threat.


Normal Action Potential (AP) Phases:

  • In the beginning of the AP (Phase 0), Sodium channels open, with rapid Sodium influx.


  • While Sodium moves into the cell, a small amount of Potassium exits the cell (Phase 1).


  • This triggers Calcium influx (Phase 2), which maintains depolarization, conductivity and cardiac contractility.


  • During repolarization (Phase 3), slow Sodium efflux occurs, while Calcium channels close, and Potassium continues to leave the cell.


  • The period where the cell remains inactive is the Resting Membrane Potential (Phase 4).


During Hyperkalemia, a greater amount of Potassium is found extracellular (>5.5mEq/L), altering the resting potential gradient, as Sodium influx is decreased and Potassium influx increases.

The main complication as a result of these electrical disturbances are lethal arrhythmias, which is why Hyperkalemia is so important to suspect. I say suspect, because otherwise, it will go untreated, and untreated means death!

Calcium does not cause intracellular Potassium influx, but it helps maintain the cell membrane AP threshold, the gradient between intracellular Potassium and extracellular Sodium, and vise versa. Because of this, Calcium Chloride or Calcium Gluconate are given along with other medications which increase Potassium influx and excess removal, such as Insulin and Dextrose, Albuterol, Loop diuretics, Sodium Bicarbonate (acidosis) and Kayexalate, often and ultimately, dialysis.



Calcium Chloride 10% has 13.6 mEq/L of elemental calcium per 1g, while 1g of Calcium Gluconate 10% has 4.65 mEq/L, but their effects on cardiac membrane stabilization are equally effective with extremely beneficial results and little to no harm, to the point that many clinicians consider Calcium treatment benign. Treatment leads to ECG normalization, but again, it does not correct the serum Potassium levels.

Here are some great links about Hyperkalemia (by our own, Dr. Brooks Walsh and our great friend Dr. Stephen W. Smith ):



  • Garrett Suchecki says:

    Awesome overview of CaCl/gluc!
    I noticed your mention of kayexalate/SPS given alongside Ca to treat hyperk. Have you seen any of this new stuff challenging the evidence base and utility of SPS for acute hyperk management?

    • Ivan Rios says:

      Yes, there are a lot of new studies showing no true effect in the treatment of Hyperkalemia. I have noticed some do it because, “that’s how it’s been done”.

  • Chris says:

    Be careful with your wording. Diuretics, kayexalate and dialysis do not cause an influx of potassium. In the acute setting, the mainstay of treatments that cause a shift are insulin/glucose, albuterol and, if profoundly acidotic, sodium bicarbonate. The utility of kayexalate is being increasingly questioned and diuretics will not do a thing if your patient is anuric, which is often the case.

    • Ivan Rios says:

      Hi Chris, thank you for your observation. I hope its clear now. My emphasis is to help understand Calcium’s mechanism in the presence of Hyperkalemia, but I have addressed the confusion.

  • Ben says:

    What in the pt’s hx argued for hyper K. Got the weakness part, but curious to know what clinical nugget could have pointed to hyper K besides weakness. Thanks

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