Hyperkalemia

A condition that result when blood potassium levels are higher than (3.5-5.0mmol/L) normal range.

Potassium is a signaling molecule in muscle contraction and cardiac function.

this may result in life threatening cardiac arrythmias and cardiac arrest.

Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L.1 Ranges are as follows:

  • 5.5-6.0 mEq/L – Mild
  • 6.1-7.0 mEq/L – Moderate
  • 7.0 mEq/L and greater – Severe

Etiology:

Hyperkalemia results from the following:

  • Decreased or impaired potassium excretion – As observed with acute or chronic renal failure (most common), potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)
  • Additions of potassium into extracellular space – As observed with potassium supplements (eg, PO/IV potassium, salt substitutes), rhabdomyolysis, and hemolysis (eg, blood transfusions, burns, tumor lysis)
  • Transmembrane shifts (ie, shifting potassium from the intracellular to extracellular space) – As observed with acidosis and medication effects (eg, acute digitalis toxicity, beta-blockers, succinylcholine)
  • Factitious or pseudohyperkalemia – As observed with improper blood collection (eg, ischemic blood draw from venipuncture technique), laboratory error, leukocytosis, and thrombocytosis
  • Pseudohyperkalemia
    • Hemolysis (in laboratory tube) most common
    • Thrombocytosis
    • Leukocytosis
    • Venipuncture technique (ie, ischemic blood draw from prolonged tourniquet application)
  • Redistribution
    • Acidosis
    • Insulin deficiency
    • Beta-blocker drugs
    • Acute digoxin intoxication or overdose
    • Succinylcholine6
    • Arginine hydrochloride
    • Hyperkalemic familial periodic paralysis
  • Excessive endogenous potassium load
    • Hemolysis
    • Rhabdomyolysis
    • Internal hemorrhage
  • Excessive exogenous potassium load
    • Parenteral administration
    • Excess in diet
    • Potassium supplements
    • Salt substitutes
  • Diminished potassium excretion
    • Decreased glomerular filtration rate (eg, acute or end-stage chronic renal failure)
    • Decreased mineral corticoid activity
    • Defect in tubular secretion (eg, renal tubular acidosis II and IV)
    • Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics)
  • Manifestations:

  • Patients may be asymptomatic or report the following:
    • Generalized fatigue
    • Weakness
    • Paresthesias
    • Paralysis
    • Palpitations
  • Assessment and Diagnositics:

    1. blood work
    2. cardiac monitoring

     

    Treatment

    1. establish IV access
    2. electrolyte supplementation such as Calcium to re-establish the normal resting and membrane potential thresholds for muscle contraction
    3. in mild cases only diuretics may be needed to enhance secretion of excess potassium.

     

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