Potassium in the blood

Reference values (norm) for potassium concentration in blood serum are 3.5-5 mmol/l (meq/l).

The body of a healthy person weighing 70 kg contains 3150 mmol of potassium (45 mmol/kg in men and 35 mmol/kg in women). Only 50-60 mmol of potassium is in the extracellular space, the rest is distributed in the cellular space. The daily intake of potassium is 60-100 mmol. Almost the same amount is excreted in the urine, and very little (2%) is excreted in the feces. Normally, the kidney excretes potassium at a rate of up to 6 mmol/(kg.day). The concentration of potassium in the blood serum is an indicator of its total content in the body, but its distribution between cells and extracellular fluid can be affected by various factors (impaired acid-base balance, increased extracellular osmolarity, insulin deficiency). Thus, with a pH shift of 0.1, one should expect a change in the potassium concentration of 0.1-0.7 mmol/l in the opposite direction.

Potassium plays a vital role in muscle contraction, heart function, nerve impulse transmission, enzymatic processes and metabolism.

When assessing the state of electrolyte balance, only very low and very high potassium concentration values that are outside the normal range are significant. In clinical conditions, hypokalemia is considered to be a potassium concentration below 3.5 mmol/l, and hyperkalemia is considered to be above 5 mmol/l.

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Regulation of potassium in the body

Potassium is the major intracellular cation, but only 2% of total body potassium is extracellular. Because most intracellular potassium is in muscle cells, total body potassium is proportional to lean body mass. The average 70-kg adult has 3,500 mEq of potassium.

Potassium is the main determinant of intracellular osmolality. The ratio of potassium in the ICF to the ECF significantly affects the polarization of cell membranes, which in turn affects many cellular processes, such as the conduction of nerve impulses and the contraction of muscle cells (including myocardial). Thus, relatively small changes in plasma potassium concentration can have significant clinical manifestations.

In the absence of factors that cause potassium movement into and out of cells, plasma potassium levels closely correlate with total body potassium levels. Given a constant plasma pH, a decrease in plasma potassium concentration from 4 to 3 mEq/L indicates a total body potassium deficiency of 100-200 mEq. A decrease in plasma potassium concentration of less than 3 mEq/L indicates a total body potassium deficiency of 200-400 mEq.

Insulin promotes movement of potassium into cells; therefore, high insulin levels decrease plasma potassium concentrations. Low insulin levels, as in diabetic ketoacidosis, promote movement of potassium out of cells, thus raising the plasma potassium concentration, sometimes even in the presence of a systemic potassium deficit. Adrenergic agonists, particularly selective β-agonists, promote movement of potassium into cells, whereas blockers and agonists promote movement of potassium out of cells. Acute metabolic acidosis promotes movement of potassium out of cells, and acute metabolic alkalosis promotes movement of potassium into cells. However, changes in plasma HCO may be more important than changes in pH; acidosis due to accumulation of mineral acids (hyperchloremic acidosis) leads to increased plasma potassium. Metabolic acidosis due to accumulation of organic acids does not cause hyperkalemia. Thus, the hyperkalemia often seen in diabetic ketoacidosis is probably due to insulin deficiency rather than acidosis. Acute respiratory acidosis and alkalosis have a greater impact on plasma potassium concentration than metabolic acidosis and alkalosis. However, plasma potassium concentration must be interpreted in the context of plasma pH (and HCO3 concentration).

Dietary potassium intake is about 40-150 mEq/L per day. At steady state, fecal losses are about 10% of intake. Urinary excretion contributes to potassium balance. When K intake is elevated (> 150 mEq K per day), about 50% of the excess potassium appears in the urine over the next few hours. Much of the remainder is transferred to the intracellular space to reduce the rise in plasma potassium. If elevated potassium intake continues, renal potassium excretion increases due to K-induced aldosterone secretion; aldosterone promotes potassium excretion. Potassium absorption from feces is probably under regulatory influence and may be reduced by up to 50% during chronic potassium excess.

When potassium intake is reduced, intracellular potassium serves as a reserve to prevent abrupt changes in plasma potassium concentration. Renal potassium conservation develops relatively slowly in response to reduced dietary potassium intake and is much less efficient than the renal ability to conserve Na. Potassium depletion is therefore a common clinical problem. Urinary potassium excretion of 10 mEq/day represents near maximal renal potassium conservation and suggests a significant potassium depletion.

Acute acidosis impairs potassium excretion, whereas chronic acidosis and acute alkalosis may promote potassium loss. Increased Na influx into the distal nephrons, as seen with high Na intake or loop diuretic therapy, promotes potassium excretion.

Pseudohypokalemia, or falsely low potassium, is sometimes seen in patients with chronic myelocytic leukemia when the white blood cell count is greater than 105/μL if the specimen is at room temperature before processing, due to potassium being taken up from the plasma by abnormal white blood cells. This can be avoided by rapidly separating the plasma or serum in the blood specimen. Pseudohyperkalemia, or falsely elevated serum potassium, is more common, usually due to hemolysis and release of intracellular potassium. To prevent this error, blood collectors should avoid drawing too quickly with a fine needle and should avoid excessive shaking of the blood specimen. Pseudohyperkalemia may also occur when the platelet count is greater than 106/μL due to increased release of potassium from platelets during clotting. In pseudohyperkalemia, the plasma (unclotted blood) potassium, unlike the serum potassium, is normal.