Potassium in the blood

The reference values (norm) of potassium concentration in the serum are 3.5-5 mmol / l (meq / l).

In the body of a healthy person with a body weight of 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 of its quantity 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 with calories. Normally, the kidney secretes potassium at a rate of up to 6 mmol / (kg.sut). The concentration of potassium in the blood serum is an indicator of its total content in the body, however, its distribution between cells and extracellular fluid can be influenced by various factors (violation of CBS, increased extracellular osmolarity, insulin deficiency). Thus, when the pH is shifted by 0.1, we should expect a change in the potassium concentration by 0.1-0.7 mmol / l in the opposite direction.

Potassium plays an important role in the processes of muscle contraction, heart activity, conduction of nerve impulses, enzymatic processes and metabolism.

In assessing the state of electrolyte balance, only very low and very high potassium concentrations are important, which go beyond the norm. In clinical conditions hypokalemia is considered a potassium concentration below 3.5 mmol / l, hyperkalemia - above 5 mmol / l.

[1], [2], [3], [4], [5], [6], [7], [8]

Regulation of potassium in the body

Potassium is the main intracellular cation, but only 2% of the total potassium in the body is in the extracellular space. Since most intracellular potassium is found in muscle cells, the total potassium content in the body is proportional to the fat-free body weight component. An average adult weighing 70 kg contains 3500 meq of potassium.

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

In the absence of factors responsible for the movement of potassium inside and out of cells, the levels of potassium in the plasma are closely correlated with the total content of potassium in the body. Considering the constant level of the pH of the plasma, a decrease in the potassium concentration in the plasma from 4 to 3 meq / l indicates a general deficit of K 100-200 meq. A decrease in the potassium concentration in the plasma of less than 3 meq / l indicates a total potassium deficiency of 200-400 meq.

Insulin promotes the movement of potassium into cells; therefore, high levels of insulin reduce the potassium concentration in the plasma. Low levels of insulin, like diabetic ketoacidosis, promote the movement of potassium from the cells, thus increasing the potassium concentration in the plasma, sometimes even with a general deficit of potassium in the body. Adrenergic agonists, especially selective 2 -agonists, promote the movement of potassium into cells, while blockers and aagonists cause potassium to move from the cells. Acute metabolic acidosis causes the movement of potassium from the cells, and acute metabolic alkalosis promotes the movement of potassium into the cells. However, changes in HCO in the plasma may be more important than a change in pH; acidosis, caused by the accumulation of mineral acids (hyperchloremic acidosis) leads to an increase in the level of potassium in the plasma. Metabolic acidosis, caused by the accumulation of organic acids, does not cause hyperkalemia. Thus, hyperkalemia, often observed in diabetic ketoacidosis, is probably caused by insulin deficiency, rather than acidosis. Acute respiratory acidosis and alkalosis give more attention to the potassium concentration in the plasma than metabolic acidosis and alkalosis. Nevertheless, the potassium concentration in the plasma should be interpreted in the context of the pH level of the plasma (and the concentration of HCO).

The intake of potassium from food is about 40-150 meq / l per day. In a stable state, losses with feces amount to about 10% of consumption. Excretion in the urine contributes to the balance of potassium. When K intake is increased (> 150 mEq K per day), about 50% excess potassium appears in the urine for the next few hours. Most of the residue passes into the intracellular space to reduce the rise in the potassium plasma level. If the increased potassium intake continues, renal excretion of potassium increases due to the aldosterone-induced secretion; aldosterone promotes the excretion of potassium. Probably, the absorption of potassium from feces is under the regulatory influence and can be reduced to 50% with a chronic excess of potassium.

When potassium intake decreases, intracellular potassium is a reserve to prevent sudden changes in potassium concentration in the plasma. Keeping the potassium by the kidneys develops relatively slowly in response to a decrease in potassium intake with food and is much less effective than the ability of the kidneys to retain Na. Thus, a decrease in the potassium level is a frequent clinical problem. Excretion of potassium in the urine of 10 meq / day represents an almost maximum retention of potassium by the kidneys and suggests a significant decrease in potassium.

Acute acidosis disrupts the excretion of potassium, while chronic acidosis and acute alkalosis can promote the excretion of potassium. The increased intake of Na in the distal nephrons, which is observed with a high intake of Na or therapy with loop diuretics, promotes the excretion of potassium.

Pseudohypokalemia, or a false low potassium level, is sometimes observed in patients with chronic myelocytic leukemia with a leukocyte count of more than 105 / μl if the sample is at room temperature before treatment, due to potassium capture from the plasma by abnormal leukocytes. This can be avoided by rapid separation of plasma or serum from blood samples. Pseudohypergalyemia, or a falsely elevated serum potassium level, is observed more often, usually due to hemolysis and the release of intracellular potassium. To prevent such an error, blood collection staff should not take the fence too fast with a thin needle, and also shake blood samples excessively. Pseudohypergalyemia can also be observed at a platelet level of more than 106 / μl due to an increased yield of potassium from platelets during clotting. In the case of pseudohypergalyemia, the level of potassium in the plasma (unticked blood), in contrast to the potassium level in the serum, is normal.