What is Hyperkalemia?
Hyperkalemia is a condition in which the concentration of potassium in the plasma exceeds 5 mmol / l. It occurs as a result of the release of potassium from the cells or a violation of potassium excretion by the kidneys.
Abnormal potassium levels are quickly signaled by ECG changes in lead II. In hyperkalemia, pointed T teeth are observed, and in hypokalemia, flattened T teeth and U waves are observed.
Causes of Hyperkalemia
Hyperkalemia occurs as a result of the release of potassium from the cells or a violation of potassium excretion by the kidneys. An increase in potassium intake is rarely the only cause of hyperkalemia, since its adaptation is rapidly increasing due to adaptation mechanisms.
Iatrogenic hyperkalemia occurs as a result of excessive parenteral administration of potassium, especially in patients with chronic renal failure.
Pseudohyperkalemia is caused by the release of potassium from the cells during blood collection. It is observed in violation of the venipuncture technique (if the tourniquet is tightened too long), hemolysis, leukocytosis, thrombocytosis. In the latter two cases, the potassium is released from the cells during the formation of a blood clot. Pseudohyperkalemia should be suspected if the patient has no clinical manifestations of hyperkalemia and there are no reasons for its development. In this case, in a properly taken blood and measurement of the concentration of potassium in the plasma, and not in the serum, this concentration should be normal.
Potassium is released from cells during hemolysis, tumor collapse syndrome, rhabdomyolysis, metabolic acidosis due to intracellular capture of hydrogen ions (except for cases of accumulation of organic anions), insulin deficiency and plasma hyperosmolarity (for example, hyperglycemia), treatment with beta-blockers (rarely occurs, but may contribute to hyperkalemia caused by other factors), the use of depolarizing muscle relaxants, such as suxametonium chloride (especially in the case of injury, burns, neuropathy) neck disease).
Exercise causes transient hyperkalemia, followed by hypokalemia.
A rare cause of hyperkalemia is familial hyperkalemic periodic paralysis. This autosomal dominant disease is caused by a single amino acid substitution in the sodium channel protein of striated muscle fibers. The disease is characterized by bouts of muscle weakness or paralysis, occurring in situations that promote the development of hyperkalemia (for example, during exercise).
Hyperkalemia is also observed in severe glycosidic intoxication due to the suppression of the activity of Na +, K + -ATPase.
Chronic hyperkalemia is almost always caused by a decrease in potassium excretion by the kidneys as a result of either a violation of its secretion mechanisms or a decrease in fluid flow to the distal nephron. The latter cause rarely causes hyperkalemia on its own, however, it may contribute to its development in patients with protein deficiency (due to a decrease in urea excretion) and hypovolemia (due to reduced intake of sodium ions and chlorine in the distal nephron).
A violation of the secretion of potassium ions occurs as a result of a decrease in the reabsorption of sodium ions or an increase in the reabsorption of chlorine ions. Both that and another leads to reduction of transepithelial potential in the cortical section of the collecting tubules.
Trimethoprim and pentamidine also reduce potassium secretion by reducing sodium reabsorption in the distal nephron. Perhaps it is the action of these drugs that explains hyperkalemia, which often occurs in the treatment of Pneumonia in AIDS patients.
Hyperkalemia is often observed in oliguric OPN due to an increase in the yield of potassium from the cells (due to acidosis and increased catabolism) and a violation of its excretion.
With chronic kidney disease, an increase in fluid intake in the distal nephron to a certain time compensates for a decrease in the number of nephrons. However, when the GFR becomes less than 10.15 ml / min, hyperkalemia occurs.
Often the cause of hyperkalemia is undiagnosed urinary tract obstruction.
Disorders of potassium excretion are also accompanied by drug nephritis, lupus nephritis, sickle cell anemia, diabetic nephropathy.
Symptoms of Hyperkalemia
The resting potential is determined by the ratio of potassium concentrations inside the cell and in the extracellular fluid. When hyperkalemia due to cell depolarization and decrease in cell excitability, muscle weakness occurs, up to paresis and respiratory failure. In addition, ammoniogenesis, the reabsorption of the ammonium ion in the thick segment of the ascending part of the loop of Henle and, consequently, the excretion of hydrogen ions are inhibited. The metabolic acidosis resulting from this aggravates hyperkalemia because it stimulates the release of potassium from the cells.
The most serious manifestations are due to the cardiotoxic effect of potassium. First, there are high pointed teeth of T. In more severe cases, the PQ interval is extended and the QRS complex expands, AV-conduction slows down, the R-tooth disappears. Expansion of the QRS complex and its merging with the T wave leads to a sinusoid-like curve. Further ventricular fibrillation and asystole occur. In general, however, the severity of the cardiotoxic effect does not correspond to the degree of hyperkalemia.
Chronic hyperkalemia is almost always associated with impaired excretion of potassium. If the cause of hyperkalemia is unclear and the patient has no manifestations of it, first of all it is necessary to suspect pseudo-hyperkalemia. Then exclude oliguric OPN and severe CKD.
When collecting the history, they clarify whether the patient took medications that affect the potassium balance, and whether hyperkalemia is associated with excess potassium intake from food.
When physical examination pay attention to signs of changes in the volume of extracellular fluid and the BCC, determine diuresis.
The severity of hyperkalemia is assessed by the totality of clinical manifestations, ECG abnormalities and plasma potassium concentrations.
With hyperkalemia, normally functioning kidneys expel at least 200 mmol of potassium per day.
In most cases, a decrease in potassium excretion is due to a violation of its secretion, which is manifested by a decrease in the transcranial gradient of potassium concentrations below 10. This is usually observed with hypoaldosteronism or with a decrease in the sensitivity of the kidneys to mineralocorticoid. Samples with mineralocorticoids (for example, with fludrocortisone) allow to clarify the cause.
For the differential diagnosis of primary adrenal insufficiency and hyporenin hypoaldosteronism determine the level of renin and aldosterone in the plasma in a standing position and lying down. Preparation for this study is carried out for 3 days. Her goal is to create moderate hypovolemia. To do this, limit sodium intake (no more than 10 mmol / day) and prescribe loop diuretics.
With a decrease in the sensitivity of the kidneys to mineralocorticoid hyperkalemia occurs due to a decrease in sodium reabsorption or an increase in chlorine reabsorption. In the first case, a decrease in the volume of extracellular fluid and a high level of renin and aldosterone in the plasma are observed, in the second – vice versa.
Hypoaldosteronism leads to severe hyperkalemia, only if combined with excess intake of potassium from food, renal failure, the release of potassium from cells, the use of drugs that violate the excretion of potassium.
Treatment depends on the degree of hyperkalemia and is determined by the concentration of potassium in the plasma, the presence of muscle weakness, changes in the ECG. Life-threatening hyperkalemia occurs with an increase in plasma potassium concentration of more than 7.5 mmol / l. At the same time, marked muscular weakness, the disappearance of the P wave, expansion of the QRS complex, ventricular arrhythmias are observed.
Emergency care is indicated for severe hyperkalemia. Its goal is to recreate a normal resting potential, move potassium into cells and increase potassium excretion. Stop the flow of potassium from the outside, cancel the drugs that violate its excretion. To reduce the excitability of the myocardium, calcium gluconate is injected, 10 ml of a 10% solution in / in for 2-3 minutes. Its action begins after a few minutes and lasts for 30.60 minutes. If 5 minutes after the administration of calcium gluconate changes on the ECG persist, the drug is re-administered at the same dose.
The movement of potassium into the cells and a temporary decrease in its concentration in the plasma contributes to insulin. 10-20 units of short-acting insulin and 25-50 g of glucose are introduced (to prevent hypoglycemia; glucose is not administered for hyperglycemia). The action lasts for several hours; already within 15-30 minutes the concentration of potassium in the blood decreases by 0.5-1.5 mmol / l.
A decrease in potassium concentration, although not as rapid, is also observed with the introduction of glucose alone (due to the secretion of endogenous insulin).
Sodium bicarbonate also promotes the movement of potassium into cells. It is prescribed for severe hyperkalemia with metabolic acidosis. The drug should be administered in the form of an isotonic solution (134 mmol / l). For this, 3 ampoules of bicarbonate are diluted in 1000 ml of 5% glucose. With CRF, sodium bicarbonate is ineffective and can lead to sodium overload and hypervolemia.
Beta2-adrenostimulyatory when administered parenterally or inhalation also contribute to the movement of potassium into the cells. The action begins after 30 minutes and lasts 2-4 hours. The concentration of potassium in plasma decreases by 0.5-1.5 mmol / l.
Diuretics, cation exchange resins and hemodialysis are also used. In normal kidney function, loop and thiazide diuretics, as well as their combination, increase the excretion of potassium. Cation-exchange resin sodium polystyrene sulfonate exchanges potassium for sodium in the gastrointestinal tract: 1 g of the drug binds 1 mmol of potassium, as a result of which 2-3 mmol of sodium are released. The drug is administered orally at a dose of 20-50 g in 100 ml of 20% sorbitol solution (to prevent constipation). The action occurs after 1-2 hours and lasts 4-6 hours. The concentration of potassium in plasma decreases by 0.5-1 mmol / l. Sodium polystyrenesulfonate can be administered as an enema (50 g of the preparation, 50 ml of 70% sorbitol solution, 150 ml of water).
Sorbitol is contraindicated in the postoperative period, especially after kidney transplantation, since it increases the risk of colon necrosis.
Hemodialysis is the fastest and most effective way to reduce the concentration of potassium in the plasma. It is indicated in the case of severe hyperkalemia with the ineffectiveness of other conservative measures, as well as in patients with acute renal failure and chronic renal failure. Peritoneal dialysis can be used to reduce the concentration of potassium in plasma, but it is significantly inferior to hemodialysis in terms of efficiency. Be sure to conduct treatment aimed at eliminating the causes of hyperkalemia. It includes diet, elimination of metabolic acidosis, increase in extracellular fluid, the appointment of mineralocorticoids.