Overview of Disorders of Potassium Concentration
Potassium is the most abundant intracellular cation, but only about 2% of total body potassium is extracellular. Because most intracellular potassium is contained within muscle cells, total body potassium is roughly proportional to lean body mass. An average 70-kg adult has about 3500 mEq of potassium.
Potassium is a major determinant of intracellular osmolality. The ratio between potassium concentration in the ICF and concentration in the ECF strongly influences cell membrane polarization, which in turn influences important cell processes, such as the conduction of nerve impulses and muscle (including myocardial) cell contraction. Thus, relatively small alterations in serum potassium concentration can have significant clinical manifestations. Total serum potassium concentration may be too high (hyperkalemia) or too low (hypokalemia). Clinical manifestations of disorders of potassium concentration can involve muscle weakness and cardiac arrhythmias.
In the absence of factors that shift potassium in or out of cells (see Overview of Disorders of Potassium Concentration : Potassium shifts), the serum potassium concentration correlates closely with total body potassium content. Once intracellular and extracellular concentrations are stable, a decrease in serum potassium concentration of about 1 mEq/L indicates a total potassium deficit of about 200 to 400 mEq. Patients with stable potassium concentration <3 mEq/L typically have a significant potassium deficit.
Factors that shift potassium in or out of cells include the following:
Insulin moves potassium into cells; high concentrations of insulin thus lower serum potassium concentration. Low concentrations of insulin, as in diabetic ketoacidosis, cause potassium to move out of cells, thus raising serum potassium, sometimes even in the presence of total body potassium deficiency.
Beta-adrenergic agonists, especially selective beta 2-agonists, move potassium into cells, whereas beta-blockade and alpha-agonists promote movement of potassium out of cells.
Acute metabolic acidosis causes potassium to move out of cells, whereas acute metabolic alkalosis causes potassium to move into cells. However, changes in serum bicarbonate concentration may be more important than changes in pH; acidosis caused by accumulation of mineral acids (nonanion gap, hyperchloremic acidosis) is more likely to elevate serum potassium. In contrast, metabolic acidosis due to accumulation of organic acids (increased anion gap acidosis) does not cause hyperkalemia. Thus, the hyperkalemia common in diabetic ketoacidosis results more from insulin deficiency than from acidosis. Acute respiratory acidosis and alkalosis affect serum potassium concentration less than metabolic acidosis and alkalosis. Nonetheless, serum potassium concentration should always be interpreted in the context of the serum pH (and bicarbonate concentration).
Dietary potassium intake normally varies between 40 and 150 mEq/day. In the steady state, fecal losses are usually close to 10% of intake. The remaining 90% is excreted in the urine so alternations in renal potassium secretion greatly affect potassium balance.
When potassium intake is > 150 mEq/day, about 50% of the excess potassium appears in the urine over the next several hours. Most of the remainder is transferred into the intracellular compartment, thus minimizing the rise in serum potassium. When elevated potassium intake continues, aldosterone secretion is stimulated and thus renal potassium excretion rises. In addition, potassium absorption from stool appears to be under some regulation and may fall by 50% in chronic potassium excess.
When potassium intake falls, intracellular potassium again serves to buffer wide swings in serum potassium concentration. Renal potassium conservation develops relatively slowly in response to decreases in dietary potassium and is far less efficient than the kidneys’ ability to conserve sodium. Thus, potassium depletion is a frequent clinical problem. Urinary potassium excretion of 10 mEq/day represents near-maximal renal potassium conservation and implies significant potassium depletion.
Acute acidosis impairs potassium excretion, whereas chronic acidosis and acute alkalosis can promote potassium excretion. Increased delivery of sodium to the distal nephrons, as occurs with high sodium intake or loop diuretic therapy, promotes potassium excretion.
Pseudohypokalemia,or falsely low serum potassium, occasionally is found when blood specimens from patients with chronic myelogenous leukemia and a WBC count >105/μL remain at room temperature before being processed because abnormal leukocytes in the sample take up serum potassium. It is prevented by prompt separation of plasma or serum in blood samples.
Pseudohyperkalemia,or falsely elevated serum potassium, is more common, typically occurring due to hemolysis and release of intracellular potassium. To prevent false results, phlebotomy personnel should not rapidly aspirate blood through a narrow-gauge needle or excessively agitate blood samples. Pseudohyperkalemia can also result from platelet count > 400,000/μL due to release of potassium from platelets during clotting; in these cases, the plasma potassium (unclotted blood), as opposed to serum potassium, is normal.