Increased intake of potassium—from excessive dietary intake, I.V. administration of penicillin G (Pfizerpen), potassium supplements, or banked whole blood—is one factor contributing to the development of hyperkalemia. Also, changes in cell membrane permeability or damage to cells from surgery, burns, massive crush injuries, cell hypoxia, acidosis, and insulin deficiency may cause potassium to shift from the intracellular space to the extracellular space. Increased serum levels of potassium may also stem from decreased renal excretion of potassium. This excretion may occur because of renal failure, decreased production and secretion of aldosterone, Addison’s disease, and the use of potassium-sparing diuretics.

When extracellular potassium concentrations increase without a significant change in intracellular potassium concentrations, the cell becomes less negative, or partially depolarized, and the resting cell membrane potential decreases. Mild elevations in extracellular potassium result in cells that repolarize faster and are more irritable. More critical elevations in extracellular potassium result in an inability of cells to repolarize and respond to electrical stimuli. Cardiac standstill, or asystole, is the most serious consequence of severe hyperkalemia.

Mild hyperkalemia may cause neuromuscular irritability, including restlessness, intestinal cramping, diarrhea, and tingling lips and fingers. Severe hyperkalemia may cause loss of muscle tone, muscle weakness, and paralysis.

Treatment depends upon the severity of hyperkalemia and the patient’s signs and symptoms. The underlying cause must be identified and the extracellular potassium concentration brought back to normal. Drug therapy to normalize potassium levels includes calcium gluconate to decrease neuromuscular irritability, insulin and glucose to facilitate the entry of potassium into the cell, and sodium bicarbonate to correct metabolic acidosis.

Oral or rectal administration of cation exchange resins, such as sodium polystyrene sulfonate (Kayexalate), may be used to exchange sodium for potassium in the intestine. In the setting of renal failure or severe hyperkalemia, dialysis may be necessary to remove excess potassium. The patient’s serum potassium levels should be monitored closely until they return to normal, and arrhythmias should be identified and managed appropriately.

Cell lysis resulting from chemotherapy can be prevented with adequate hydration before,
during, and after the administration of the chemotherapy. If the patient isn’t able to tolerate oral fluids, I.V. fluids may be given.

Factors contributing to hypokalemia include increased loss of body potassium, increased entry of potassium into cells, and reduced potassium intake. Shifts in potassium from the extracellular space to the intracellular space may be caused by alkalosis, especially respiratory alkalosis. Intracellular uptake of potassium is also increased by catecholamines. Although rare, a dietary deficiency may contribute to hypokalemia in an elderly person. The condition is also seen in patients with alcoholism, hepatic disease, and anorexia nervosa. Potassium is also lost during diabetic ketoacidosis because of osmotic diuresis.

GI and renal disorders are the most common causes of potassium loss from body stores. GI losses of potassium are associated with laxative abuse, intestinal fistulae or drainage tubes, diarrhea, vomiting, and continuous nasogastric drainage.

Renal loss of potassium is related to increased secretion of potassium by the distal tubule. Diuretics, a low serum magnesium concentration, and excessive aldosterone secretion may cause urinary loss of potassium. In addition, several antibiotics, including gentamicin (Garamycin) and amphotericin B (Fungizone), are known to cause hypokalemia.

When extracellular potassium levels decrease rapidly and intracellular potassium concentration doesn’t change, the resting membrane potential becomes more negative and the cell membrane becomes hyperpolarized. The cardiac effects of hypokalemia are related to these changes in membrane excitability. Ventricular repolarization is delayed because potassium contributes to the repolarization phase of the action potential. Hypokalemia can cause dangerous ventricular
arrhythmias and increases the risk of digoxin toxicity.

The most common symptoms of hypokalemia are caused by neuromuscular and cardiac effects, including smooth muscle atony, skeletal muscle weakness, and cardiac arrhythmias. Loss of smooth muscle tone results in constipation, intestinal distention, nausea, vomiting, anorexia, and paralytic ileus. Skeletal muscle weakness occurs first in the larger muscles of the arms and legs and eventually affects the diaphragm, causing respiratory arrest.

Cardiac effects of hypokalemia include arrhythmias, such as bradycardia, atrioventricular (AV) block, and paroxysmal atrial tachycardia. Delayed depolarization results in characteristic changes on the ECG.

The underlying causes of hypokalemia should be identified and corrected. Acid-base imbalances should be corrected, potassium losses replaced, and further losses prevented. Encourage intake of foods and fluids rich in potassium. Oral or I.V. potassium supplements may be administered. The patient’s serum potassium levels should be monitored closely until they return to normal, and cardiac arrhythmias should be identified and managed appropriately.

The most common causes of hypercalcemia include excess vitamin D intake; bone metastasis and calcium resorption associated with cancers of the breast, prostate, and cervix; hyperparathyroidism; sarcoidosis; thyrotoxicosis; thiazide diuretic therapy; and many parathyroid hormone–producing tumors.

In hypercalcemia, calcium is found inside cells in greater abundance than normal. The cell membrane becomes refractory to depolarization as a result of a more positive action potential, and a stronger stimulus is needed to cause a response in the cell membrane. This loss of cell membrane excitability causes many of the cardiac symptoms seen in patients with hypercalcemia.

Both ventricular depolarization and repolarization are accelerated. The patient may experience bradyarrhythmias and varying degrees of AV block.

Common signs and symptoms of hypercalcemia include anorexia, nausea, constipation, lethargy, fatigue, polyuria, and weakness. Behavioral changes may also occur. Renal calculi may form as precipitates of calcium salts. Impaired renal function commonly occurs. A reciprocal decrease in serum phosphate levels commonly accompanies elevated levels of serum calcium.