Which of the following statement(s) is/are true concerning abnormalities in serum potassium?

c. Temporary treatment of hyperkalemia includes administration of calcium, sodium bicarbonate, or glucose and insulin

d. Alterations in membrane potentials reflected in cardiac and skeletal muscle are common results of both hypo-and hyperkalemia

Potassium is the major intracellular cation and is a major determinant of intracellular osmolality. Because of the large differences between intracellular and extracellular potassium concentrations, a transmembrane potential is generated. Alterations in potassium concentration gradient (both hyper- and hypokalemia) have profound effects on transmembrane potential and consequently on cellular function. This is especially true for cardiac, skeletal, and smooth muscle. Extracellular potassium concentration is primarily determined by renal excretion. About 90% of ingested potassium is secreted by the urine. Hyperkalemia therefore rarely develops from excessive potassium intake in the absence of renal insufficiency, since the capacity for renal potassium excretion is large. In the surgical patient, diminished renal function is perhaps the most common problem leading to hyperkalemia. Both chronic and acute renal failure result in the deficit in potassium excretion. Hyperkalemia can also be associated with cellular disruption, such as with crush injuries or lysed erythrocytes in large hematomas or after massive blood transfusion. The clinical manifestations of hyperkalemia are primarily related to membrane depolarization. The most life-threatening manifestations are related to the cardiac effects of membrane depolarization. Mild hyperkalemia results in peaked T-waves on the EKG and may cause parethesia and weakness. More severe forms of hyperkalemia cause flattened P-waves, prolongation of the QRS complex, and deep Swaves on EKG. Ventricular fibrillation and cardiac arrest may follow. Severe hyperkalemia with EKG abnormalities requires urgent treatment. Rapid infusion of 10% to 20% calcium gluconate may reduce the effects of hyperkalemia on membrane potentials. Administration of sodium bicarbonate is another temporary measure. The increase in serum sodium antagonizes the effects of hyperkalemia on the membrane potential, whereas the increase in extracellular pH shifts potassium into the cells. Movement of potassium into the intracellular compartment can also be achieved by giving insulin and glucose.

 Hypokalemia is usually caused by total body potassium depletion secondary to the decreased potassium intake, increased extra-renal potassium losses, or increased renal potassium losses. Decreased serum potassium levels may also be secondary to redistribution of potassium into the intracellular space. Symptoms of hypokalemia, like those of hyperkalemia, are manifested by disturbances in membrane potentials. As potassium levels fall below 2.5mEq/L, muscle weakness is common. The primary treatment of hypokalemia is potassium replacement. The route and rate of potassium replacement depends on the presence and severity of symptoms. A reduction in serum potassium of 1mEq/L represents a total body potassium deficiency of 100 to 200 mEq.