Causes of elevated potassium (hyperkalemia)

Causes of hyperkalemia (increased potassium in the blood):

• decreased excretion of potassium by the kidneys in acute and chronic renal failure, as well as occlusion of renal vessels;
• acute dehydration;
• extensive injuries, burns or major surgeries, especially against the background of previous serious 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 starting insulin therapy;
• prescribing potassium-sparing diuretics, such as triamterene, spironolactone.

The above causes of hyperkalemia are based on three main mechanisms: increased potassium consumption, the transfer of potassium from the intracellular to the extracellular space, and a decrease in its loss.

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

The pathogenetic mechanism associated with increased transfer of potassium from the intracellular to the extracellular space occurs in acidosis, prolonged compression syndrome, tissue hypoxia, insulin deficiency and overdose of cardiac glycosides.

Pseudohyperkalemia may be caused by hemolysis when taking blood for analysis (applying a tourniquet for more than 2 minutes). If blood is taken in a glass test tube, 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 coagulation in the test tube.

Potassium losses are reduced in renal failure, hypoaldosteronism, diuretics that block distal tubular potassium secretion, and primary defects in renal tubular potassium secretion. Heparin, even in low doses, partially blocks aldosterone synthesis and can cause hyperkalemia (probably due to impaired tubular sensitivity to aldosterone).

Particularly high potassium levels are observed in acute renal failure, in particular in nephronephrosis caused by poisoning and crush syndrome, which is caused by a sharp decrease (to almost complete cessation) in renal excretion of potassium, acidosis, increased protein catabolism, hemolysis, and, in crush syndrome, muscle tissue damage. In this case, the potassium content in the blood can reach 7-9.7 mmol/l. The dynamics of an increase in potassium in the blood of patients with acute renal failure is of great importance in clinical practice. In uncomplicated cases of acute renal failure, the concentration of potassium in the blood plasma increases by 0.3-0.5 mmol/(l/day), after an injury or complex operation - by 1-2 mmol/(l/day), however, a very rapid increase is also possible. Therefore, monitoring the dynamics of kalemia 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 paresthesia and cardiac arrhythmias. Threatening symptoms of potassium intoxication include collapse, bradycardia, and clouding of consciousness. Changes in the ECG occur when the potassium concentration is above 7 mmol/l, and when its concentration increases to 10 mmol/l, intraventricular block with ventricular fibrillation occurs, and at a concentration of 13 mmol/l, the heart stops in diastole. As the potassium content in the blood serum increases, the nature of the ECG gradually changes. First, tall, pointed T waves appear. Then, ST segment depression, first-degree atrioventricular block, and widening of the QRS complex develop. Finally, due to further widening of the QRS complex and its fusion with the T wave, a biphasic curve is formed, indicating approaching ventricular asystole. The rate of such changes is unpredictable, and sometimes only a few minutes pass from the initial ECG changes to dangerous conduction disturbances or arrhythmias.