POTASSIUM HOMEOSTASIS


I. Hypokalemia:

  1. Causes: vomiting, diuretics, hyperaldo (liver failure, CHF, Cushing's), diarrhea, renal tubular disease
  2. Effects: U waves bigger than T's on ECG; ventricular ectopy
  3. Treatment:
    1. If severe, potassium replacement IV (40-80mEq in 500ml D5W IV over 3-6h with cardiac monitor; max. 0.5 mEq/kg/h up to 30mEq/h in adults)
    2. Potassium replacement PO (40-80mEq in divided doses)

II. Hyperkalemia:

  1. Causes:
    1. Reduced kaliuresis
      1. Reduced GFR from any cause
      2. Reduced tubular potassium secretion: Hypoaldosteronism (from Addison's disease, etc.) or potassium-sparing diuretics
    2. Shifts between fluid compartments
      1. Acidosis
      2. Cell destruction (tumor lysis, burns, hemolysis, etc.)
      3. Hypoinsulinemia, especially with hyperglycemia
    3. Exogenous potassium administration with decreased ability to excrete (potassium supplements, transfusions)
    4. Digitalis (?)
  1. Effects-Primarily cardiac
  1. At 6.5 mEq/L: Peaked T waves on ECG
  2. At 7-8 mEq/L: Increase in PR interval then loss of P wave and widening of QRS
  3. At 8-10mEq/L: Asystole
  1. Management options
  1. Treatments that stabilize cardiac myocytes and reduce likelihood of serious arrhythmias (note-May unmask digoxin toxicity)
    1. Calcium gluconate
    2. Calcium chloride
  2. Treatments that rapidly move potassium from serum to intracellular space
    1. IV (glucose + regular insulin)
    2. IV Sodium bicarbonate
    3. Albuterol (inhaled?)
  3. Treatments to reduce total body potassium
    1. Hemodialysis (in most severe cases)
    2. Sodium polystyrene sulfonate (Kayexelate) PO or PR
      1. Can also cause sodium overload
      2. Can cause constipation, so often given with sorbitol, although the combination may be associated with colonic necrosis
      3. May not actually result in clinically significant reduction of serum potassium concentration (J. Am. Soc. Nephrol. 21:733, 2010-JW)
    3. Diuretics