Hyperpotassemia

Description:

The hyperpotassemia is a state at which potassium concentration in plasma exceeds 5 mmol/l. It results from a potassium exit from cells or disturbance of removal of potassium kidneys.

About disturbances of level of potassium changes of an ECG in assignment of II quickly signal. At a hyperpotassemia the pointed T teeth are observed, and at a hypopotassemia - the flattened teeth of T and a wave of U.

Hyperpotassemia symptoms:

Rest potential is defined by a ratio of potassium concentrations in a cell and in extracellular liquid. At a hyperpotassemia owing to depolarization of cells and decrease in excitability of cells there is a muscular weakness, up to paresis and respiratory insufficiency. Besides, the ammoniogenesis, an ammonium ion reabsorption in a thick segment of the ascending part of a Henle's loop and, therefore, removal of ions of hydrogen is oppressed. The metabolic acidosis arising at the same time aggravates a hyperpotassemia as stimulates a potassium exit from cells.

The most serious manifestations are caused by cardiotoxic effect of potassium. At first there are high pointed T. V teeth more hard cases the interval of PQ is extended and the QRS complex extends, AV-carrying out is slowed down, the tooth of River disappears. Expansion of the QRS complex and its merge to a tooth of T leads to formation of the curve reminding a sinusoid. Further there are a fibrillation of ventricles and an asystolia. In general, however, expressiveness of cardiotoxic action does not correspond to hyperpotassemia degree.

Hyperpotassemia reasons:

The hyperpotassemia results from a potassium exit from cells or disturbance of removal of potassium kidneys. Increase in consumption of potassium seldom is the only reason of a hyperpotassemia as thanks to adaptable mechanisms its removal quickly increases.

The iatrogenic hyperpotassemia results from excess parenteral administration of potassium, especially at patients with HPN.

The pseudo-hyperpotassemia is caused by a potassium exit from cells during blood capture. It is observed at disturbance of the equipment of a venipuncture (if the plait is too long tightened), hemolysis, a leukocytosis, a thrombocytosis. In the last two cases potassium comes out cells at formation of blood clot. The pseudo-hyperpotassemia should be suspected if the patient has no clinical manifestations of a hyperpotassemia and there are no reasons for its development. At the same time in correctly taken blood and measurement of potassium concentration in plasma, but not in serum this concentration has to be normal.

Potassium exit from cells is observed at hemolysis, a syndrome of disintegration of a tumor, a rabdomioliza, a metabolic acidosis owing to intracellular capture of ions of hydrogen (except for cases of accumulation of organic anions), insufficiency of insulin and hyperosmolality of plasma (for example, at a hyperglycemia), treatment by beta adrenoblockers (arises seldom, but can promote the hyperpotassemia caused by other factors), use of the depolarizing muscle relaxants, for example chloride succinylcholine (especially at an injury, burns, neuromuscular diseases).

The exercise stress causes a passing hyperpotassemia after which there can be a hypopotassemia.

The rare reason of a hyperpotassemia - family giperkaliyemichesky periodic paralysis. This autosomal and dominant disease is caused by single amino-acid replacement in protein of a natrium channel of cross-striped muscle fibers. The disease is characterized by the attacks of muscular weakness or paralysis arising in the situations promoting development of a hyperpotassemia (for example, at an exercise stress).

The hyperpotassemia is observed also at heavy glikozidny intoxication owing to suppression of activity of Na +, To +-Atfazy.

The chronic hyperpotassemia is almost always caused by decrease in removal of potassium kidneys as a result of either disturbance of mechanisms of its secretion, or reduction of intake of liquid in distal departments of nephron. The last reason seldom independently leads to a hyperpotassemia, however can promote its development in patients with proteinaceous insufficiency (because of decrease in excretion of urea) and a hypovolemia (because of reduced receipt of ions of sodium and chlorine in distal departments of nephron).

Disturbance of secretion of potassium ions results from reduction of a reabsorption of ions of sodium or increase in a reabsorption of ions of chlorine. Both leads to reduction of transepithelial potential in cortical department of collective tubules.

Trimethoprimum and pentamidine reduce also secretion of potassium due to reduction of a reabsorption of sodium in distal departments of nephron. Perhaps, the hyperpotassemia which is often arising at treatment of pneumocystic pneumonia at patients with AIDS is explained by effect of these drugs.

The hyperpotassemia is often observed at oligurichesky OPN owing to increase in an exit of potassium from cells (because of acidosis and the strengthened catabolism) and disturbances of its excretion.

At HPN increase in intake of liquid in distal departments of nephron till certain time compensates decrease in amount of nephrons. However when SKF becomes less than 10,15 ml/min., there is a hyperpotassemia.

Often not diagnosed obstruction of uric ways appears the reason of a hyperpotassemia.

Medicinal nephrite, lupoid nephrite, drepanocytic anemia, diabetic nephropathy are also followed by disturbance of excretion of potassium.

Treatment of the Hyperpotassemia:

Treatment depends on degree of a hyperpotassemia and is defined by potassium concentration in plasma, existence of muscular weakness, changes on an ECG. The life-threatening hyperpotassemia arises at increase in potassium concentration in plasma more than 7,5 mmol/l. At the same time the expressed muscular weakness, disappearance of a tooth P, expansion of the QRS complex, ventricular arrhythmias are observed.

Acute management is shown at a heavy hyperpotassemia. Its purpose - a reconstruction of normal rest potential, moving of potassium to cells and strengthening of removal of potassium. Stop intake of potassium from the outside, cancel the drugs breaking its removal. For decrease in excitability of a myocardium enter a gluconate of calcium, 10 ml of 10% of solution in/in within 2-3 min. Its action begins several minutes later and continues within 30.60 min. If in 5 min. after introduction of a gluconate of calcium of change on an ECG remain, administer the drug repeatedly in the same dose.

Moving of potassium to cells and temporary decrease in its concentration in plasma are promoted by insulin. Enter 10-20 pieces of insulin of short action and 25-50 g of glucose (for the prevention of a hypoglycemia; at a hyperglycemia glucose is not entered). Action continues several hours, within 15-30 min. potassium concentration in blood decreases by 0,5-1,5 mmol/l.

Decrease in potassium concentration, though not so bystry, is observed also at administration only of glucose (due to secretion of endogenous insulin).

Sodium bicarbonate also also promotes moving of potassium to cells. It is appointed at a heavy hyperpotassemia with a metabolic acidosis. The drug should be administered in the form of isotonic solution (134 mmol/l). For this purpose 3 ampoules of bicarbonate dissolve 5% of glucose in 1000 ml. At HPN sodium bicarbonate is ineffective and can lead to an overload sodium and hypervolemias.

Beta2-adrenostimulyatora at parenteral or inhalation administration also promote moving of potassium to cells. Action begins in 30 min. and continues 2-4 h. Potassium concentration in plasma decreases by 0,5-1,5 mmol/l.

Apply also diuretics, cation-exchange resins and a hemodialysis. At normal function of kidneys loopback and thiazide diuretics, and also their combination increase potassium removal. Cation-exchange resin polystyrene sulphonate of sodium exchanges in a GIT potassium for sodium: 1 g of drug connects 1 mmol of potassium, 2-3 mmol of sodium are as a result released. Drug is appointed inside in a dose of 20-50 g in 100 ml of 20% of solution of sorbitol (for the prevention of a lock). Action comes in 1-2 h and lasts 4-6 h. Potassium concentration in plasma decreases by 0,5-1 mmol/l. Polystyrene sulphonate of sodium can be entered in the form of an enema (50 g of drug, 50 ml of 70% of solution of sorbitol, 150 ml of water).

Sorbitol is contraindicated in the postoperative period, especially after transplantation of a kidney as it increases risk of a necrosis of a large intestine.

Hemodialysis - the most bystry and effective way of decrease in potassium concentration in plasma. It is shown in case of a heavy hyperpotassemia at inefficiency of other conservative actions, and also the patient with OPN and HPN. For decrease in potassium concentration in plasma it is possible to use peritoneal dialysis, however by efficiency it considerably concedes to a hemodialysis. Carry surely out the treatment directed to elimination of the reason of a hyperpotassemia. It includes a diet, elimination of a metabolic acidosis, increase in volume of extracellular liquid, purpose of mineralokortikoid.