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April 2005, Volume 35 Number 4 , p 12 - 12


  • Judy Sweeney RN, MSN




    My patient, admitted with worsening heart failure, was receiving digoxin and furosemide. As his respiratory acidosis and volume overload resolved, his serum potassium dropped from 4.2 to 3 mEq/liter in 24 hours. Why did he become hypokalemic so fast?—T.K., MASS.

    Judy Sweeney, RN, MSN, replies: Normally, extracellular levels of potassium are relatively small (3.5 to 5 mEq/liter) compared with intracellular levels (about 150 mEq/liter), so the serum lab value for potassium constitutes less than 2% of the total body content.

    Although your patient's serum potassium level was initially normal, remember that changes in pH and hydrogen ion concentration cause potassium to shift between the extracellular and intracellular spaces. Because of these factors, acidosis causes a relative excess of extracellular potassium.

    When your patient was experiencing respiratory acidosis, potassium shifted out of cells into the extracellular fluid as it exchanged with hydrogen ions. Moving hydrogen ions into cells helped correct the acidosis by increasing pH. When the acidosis resolved and the extracellular pH returned to normal, some potassium returned to the cells, creating a relative deficiency of potassium in extracellular fluid. This, coupled with renal potassium losses from furosemide-induced diuresis, helps to explain your patient's hypokalemia.

    Other possible causes of hypokalemia include:

    * increased aldosterone production, which enhances potassium excretion in the urine

    * vomiting or diarrhea, resulting in volume depletion and metabolic alkalosis; both promote urinary excretion of potassium.

    Signs and symptoms of hypokalemia include fatigue, myalgia, and muscle weakness. More severe hypokalemia can cause paralysis, respiratory failure, cardiac arrhythmias, and hypotension. Early ECG changes include T-wave flattening or inversion, prominent U waves, and ST-segment ...

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