Potassium Imbalance

Potassium, a cation that is the dominant cellular electrolyte, facilitates contraction of both skeletal and smooth muscles - including myocardial contraction - and figures prominently in nerve impulse conduction, acid base balance, enzyme action, and cell-membrane function. Because serum potassium level has such a narrow range (3.5 to 5 mEq/L), a slight deviation in either direction can produce profound clinical consequences.

Paradoxically, both hypokalemia (potassium deficiency) and hyperkalemia (potassium excess) can lead to muscle weakness and flaccid paralysis because both create an ionic imbalance in neuromuscular tissue excitability. Both conditions also diminish excitability and conduction rate of the heart muscle, which may lead to cardiac arrest.

Causes

There are a number of possible causes of potassium imbalance.

Hypokalemia

Because many foods contain potassium, hypokalemia rarely results from a dietary deficiency. Instead, potassium loss results from:

• excessive GI or urinary losses, such as vomiting, gastric suction, diarrhea, dehydration, anorexia, or chronic laxative abuse
• trauma (injury, burns, or surgery), in which damaged cells release potassium, which enters serum or extracellular fluid to be excreted in the urine
• chronic renal disease, with tubular potassium wasting
• certain drugs, especially potassium-wasting diuretics, steroids, and certain sodium-containing antibiotics (carbenicillin)
• acid-base imbalances, which cause potassium shifting into cells without true depletion in alkalosis
• prolonged potassium-free I.V. therapy
• hyperglycemia, causing osmotic diuresis and glycosuria
• Cushing's syndrome, primary hyper­aldosteronism, excessive ingestion of licorice, and severe serum magnesium deficiency

Hyperkalemia

Generally, hyperkalemia results from the kidneys' inability to excrete excessive amounts of potassium infused I.V. or administered orally; from decreased urine output, renal dysfunction, or renal failure; or from the use of potassium-sparing diuretics, such as triamterene, by patients with renal disease. It may also result from any injuries or conditions that release cellular potassium or favor its retention, such as burns, crushing injuries, failing renal function, adrenal gland insufficiency, dehydration, or diabetic acidosis.

Signs and symptoms

• Weakness and paralysis;
• Dangerously rapid, irregular heartbeat or slow heartbeat (sometimes);
• Nausea and diarrhea.

Diagnosis

• Hypokalemia: serum potassium levels < 3.5 mEq/L.
• Hyperkalemia: serum potassium levels > 5 mEq/L.

Additional tests may be necessary to determine the underlying cause of the imbalance.

Treatment

Potassium imbalances are treated as follows.

Hypokalemia

Replacement therapy with potassium chloride (I.V. or by mouth) is the primary treatment of hypokalemia. When diuresis is necessary, spironolactone, a potassium-sparing diuretic, may be administered concurrently with a potassium-wasting diuretic to minimize potassium loss.

Hypokalemia can be prevented by giving a maintenance dose of potassium I.V. to patients who may not take anything by mouth and to others predisposed to potassium loss.

Hyperkalemia

For management of hyperkalemia, rapid infusion of 10% calcium gluconate decreases myocardial irritability and temporarily prevents cardiac arrest but doesn't correct serum potassium excess; it's also contraindicated in patients receiving a digitalis glycoside.

As an emergency measure, sodium bicarbonate I.V. increases pH and causes potassium to shift back into the cells. Insulin and 10% to 50% glucose I.V. also move potassium back into cells. Infusions should be followed by dextrose 5% in water because infusion of 10% to 15% glucose will stimulate secretion of endogenous insulin.

Sodium polystyrene sulfonate (Kayexalate) with 70% sorbitol produces exchange of sodium ions for potassium ions in the intestine. Hemodialysis or peritoneal dialysis also aids in removal of excess potassium.