Potassium

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Normal: 3.5 to 5.0 mEq/L (3.5 to 5.0 mmol/L)

Physiology:

The major physiological role of potassium is in regulating muscle and nerve excitability. Potassium is not conserved by the body; the kidneys excrete about 40 mEq/L per 24 hours. Potassium is required for the synthesis of lean body tissue, about 3 mEq/g of nitrogen is needed for anabolism. Serum potassium has a narrow range, death occurs at values outside it.

Empiric daily requirement

Adults: 60 to 200 mEq/day

Infants/children: 2 to 4 mEq/kg/day

Hypokalemia: levels below 3.5 mEq/L.

Causes:

•	Increased renal excretion, often due to diuretics.

•	GI potassium loss, due to vomiting, diarrhea, gastric suction and fistulas.

•	Inadequate oral or parenteral intake or inadequate replacement in TPN solutions.

•	Starvation

•	Hyperaldosteronism

•	Medications: corticosteroids, amphotericin B and diuretics.

Assessment:

Skeletal muscle weakness is often seen, with severe depletion leading to decreased reflexes and paralysis. Cardiovascular symptoms include rhythm disturbances and hypotension. Hypokalemic patients become more sensitive to the toxic effects of digoxin. Renal symptoms include inability to concentrate urine and nephropathy.

Labs:

Serum potassium below 3.5 mEq/L. Frequently the arterial blood gas values show a metabolic alkalosis (pH > 7.45 and HCO3 > 26 to 30 mEq/L) and potassium is shifted into the cells.

Correction:

Replace orally if possible. If oral replacement is not possible, give intravenous potassium supplements. The administration rate of IV potassium should not exceed 20 mEq/hr.

TPN correction:

A TPN solution should not be utilized for primary treatment of hypokalemia. The potassium content per liter of TPN solution should not exceed 40 mEq. If additional potassium is necessary it should be administered via another route, e.g. IV piggybacks.

Hyperkalemia: levels exceeding 5.0 mEq/L.

Causes:

•	Decreased potassium excretion due to renal disease.

•	Excess potassium intake.

•	Shift of potassium from cells due to metabolic acidosis.

•	Hyperkalemia may be caused by potassium shifts from cells as a result of cell breakdown from trauma, burns or hemolysis.

•	Metabolic acidosis and hyperglycemia resulting from insulin deficiency may pull potassium from the cells.

•	Addison's disease

•	Medications: potassium-sparing diuretics, ACE inhibitors, NSAIDs, beta-blockers, heparin and trimethoprim.

Assessment:

The hyperkalemic signs and symptoms of principle concern involve the cardiovascular system. The include cardiac dysrhythmias, bradycardia, hypotension and, in severe cases, cardiac arrest. GI symptoms include hyperactivity, nausea, diarrhea and abdominal cramps.

Labs:

Serum potassium above 5.0 mEq/L. Blood gas values indicative of metabolic acidosis (pH < 7.35 and HCO3 < 20 mEq/L).

Correction:

If excess is mild eliminate the cause of excess and allow potassium to return within normal limits. If there is a moderate potassium excess administer a hypertonic glucose IV infusion with insulin (particularly for insulin-deficient patients) to shift potassium into the cell. Insulin aids in moving potassium into the cells, whereas the glucose helps prevent hypoglycemia. Administer sodium bicarbonate to patients with metabolic acidosis to shift potassium back into the cells. If the excess is severe treat with an infusion of calcium gluconate. Patients on digoxin should be monitored for digitalis toxicity if calcium gluconate is administered.

TPN correction:

Discontinue the current TPN infusion if it contains potassium and begin an infusion of D10NS at the current TPN infusion rate. Reorder a TPN solution without potassium and continue to hold potassium from the TPN solution and all other intravenous fluids until the serum potassium returns to normal.