The causes of potassium elevation (hyperkalemia)

Causes of hyperkalemia (increased potassium in the blood):

• a decrease in the excretion of potassium by the kidneys in acute and chronic renal failure, as well as the occlusion of renal vessels;
• acute dehydration;
• extensive injuries, burns or major surgery, especially against the background of previous severe illnesses;
• severe metabolic acidosis and shock;
• chronic adrenal insufficiency (hypoaldosteronism);
• rapid infusion of a concentrated potassium solution containing more than 50 mmol / L potassium (approximately 0.4% potassium chloride solution);
• oliguria or anuria of any origin;
• diabetic coma before the onset of insulin therapy;
• the appointment of potassium-sparing diuretics, for example triamterene, spironolactone.

At the heart of the above causes of hyperkalemia are three main mechanisms: increased potassium intake, the transition of potassium from the intracellular to the extracellular space and the reduction of its losses.

Increased potassium intake usually only contributes to the development of hyperkalemia. Most often it is iatrogenic (in patients receiving intravenous fluids of solutions with a high potassium content and / or in patients with impaired renal function). To this group of reasons also include diets with a high content of potassium, uncontrolled use of potassium salt of penicillin in large doses.

The pathogenetic mechanism associated with an enhanced transition of potassium from the intracellular to the extracellular space occurs in acidosis, long-term compression syndrome, tissue hypoxia, insulin deficiency, and overdose of cardiac glycosides.

Pseudohypergalyemia can be caused by hemolysis when taking blood for analysis (application of a tourniquet over 2 min). If blood is taken into a glass vial, then such changes can be detected in 20% of blood samples. With leukocytosis (more than 50 × 10 ⁹ / l) and thrombocytosis (1000 × 10 ⁹ / L), pseudohyperkalemia is also possible due to the release of potassium during blood clotting in vitro.

Loss of potassium decreases with renal failure, hypoaldosteronism, the intake of diuretics that block the secretion of potassium by distal tubules, and with primary defects of tubular secretion of potassium by the kidneys. Heparin, prescribed even in low doses, partially blocks the synthesis of aldosterone and can cause hyperkalemia (probably due to a violation of the sensitivity of the tubules to aldosterone).

Especially high content of potassium is observed in acute renal failure, in particular in necro-nephroses caused by poisonings and long-term compression syndrome, which is caused by a sharp decrease (to almost complete cessation) of renal excretion of potassium, acidosis, increased protein catabolism, hemolysis, and with prolonged compression syndrome - damage to muscle tissue. At the same time, the content of potassium in the blood can reach 7-9.7 mmol / l. The dynamics of potassium increase in blood in patients with acute renal insufficiency plays an important role in clinical practice. In uncomplicated cases of acute renal insufficiency, the concentration of potassium in the blood plasma increases by 0.3-0.5 mmol / l, after a trauma or complicated operation - by 1-2 mmol / L, but very possible its rapid ascent. Therefore, monitoring the dynamics of potassium in patients with acute renal failure is of great importance; it should be carried out at least once a day, and in complicated cases even more often.

Hyperkalemia is clinically manifested by paresthesias, cardiac arrhythmias. The threatening symptoms of potassium intoxication include collapse, bradycardia, dullness of consciousness. Changes in the ECG occur when the potassium concentration is above 7 mmol / l, and with an increase in its concentration to 10 mmol / l, an intraventricular blockade with ventricular fibrillation occurs, at a concentration of 13 mmol / l, the heart stops in diastole. As the potassium content in the blood serum increases, the character of the ECG gradually changes. First, high pointed tars T appear. Then, depression of the ST segment, atrioventricular blockade of the 1st degree and expansion of the QRS complex develop. Finally, due to the further expansion of the QRS complex and its fusion with the T wave, a two-phase curve is formed, indicating an approaching ventricular asystole. The rate of such changes is unpredictable, and from initial ECG changes to dangerous conduction disturbances or arrhythmias sometimes take only a few minutes.