What is hyperkalemia. Is hyperkalemia, symptoms of excessive calcium secretion and its correction so dangerous? How does hyperkalemia work in the kidneys?

Hyperkalemia is an increase in the content of potassium in the blood above 5 mmol / l. It appears when there is an increased exit of ions from cells or a violation of their excretion by the kidneys. An excess of this electrolyte leads to a violation of the conduction of the myocardium, and with a sharp increase in the level, cardiac arrest is possible. Learn more about the causes of hyperkalemia, its symptoms and treatment methods in this article.

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Potassium in the body regulates all the functions of the myocardium: excitability, automatism, conduction of impulses and contraction of muscle fibers. Normally, even with increased intravenous administration of potassium salts, they are quickly excreted by the kidneys without causing significant changes in the electrolyte composition of the blood.

In diseases of the kidneys, and especially with low filtration capacity, a number of medications can cause hyperkalemia. These include:

• potassium preparations in tablets (Kalipos prolongatum, Caldium);
• infusion solutions;
• (Triampur, Veroshpiron);
• (Enap, Kapoten);
• angiotensin receptor blockers (Valsakor, Candesar);
• non-steroidal anti-inflammatory drugs (Ibuprom, Naproxen, Rancelex);
• cytostatics (Cyclosporin).

Hyperkalemia can be caused by:

• with autoimmune diseases, infections, transfusion of incompatible blood, poisoning with hemolytic poisons;
• tissue breakdown due to a malignant tumor;
• damage to muscle fibers in trauma, dermatomyositis;
• extensive burns;
• increased acidity of the blood (acidosis);
• insulin deficiency in diabetes mellitus;
• the use of beta-blockers, muscle relaxants, against the background of metabolic disorders or potassium excretion;
• congenital disorder of the structure of sodium channels (hyperkalemic paralysis), characterized by a sharp weakening of the limbs during physical activity;
• heatstroke;
• dehydration;
• diseases of the endocrine system: Addison's disease, pseudohypoaldosteronism;
• sickle cell anemia;
• medicinal and autoimmune nephritis;
• urolithiasis, prostate hypertrophy, obstructing the outflow of urine.

A stable chronic increase in potassium in the blood in almost all cases is caused by a decrease in its excretion by the kidneys. In acute renal failure, there is an increased release of it from the cells due to the active breakdown of proteins and acidification of the blood, and in the chronic form of the pathology, hyperkalemia is explained by the weak filtering ability of nephrons.

Symptoms in adults and children

For a long time, hyperkalemia does not manifest itself clinically, and then, when a level of 6-8 mmol / l is reached, patients experience:

• sharp muscle weakness up to paralysis of the limbs (often ascending, sluggish);
• violations of the clarity of speech;
• apathy, drowsiness;
• dizziness;
• shortness of breath, with an increase in the concentration of ions, respiratory failure appears;
• feeling of interruptions in the work of the heart;
• nausea;
• increased sweating;
• decrease in urine output;
• pain in the chest, abdomen;
• , turning into bradycardia or;
• inhibition of intestinal peristalsis.

In newborns, hyperkalemia is associated with functional immaturity of the renal tubules, late cord ligation, severe acidosis, or hemolysis of the blood.

A feature of the course of pathology in young children is the appearance of the first signs when the concentration of potassium exceeds 7 mmol / l. Frequent regurgitation, vomiting, adynamia, lethargy are noted, the rhythm of heart contractions, reflexes and intestinal motility are disturbed.

Watch the video about the importance of potassium in the human body:

ECG indications

The most severe manifestations of hyperkalemia are associated with impaired conduction in the myocardium. The following typical signs appear on the ECG:

• high and sharp T, shortening of ST;
• PQ extension;
• expansion of the ventricular complex and subsequent fusion with T;
• decrease in atrioventricular conduction;
• gradual disappearance of the atrial wave.

With the progression of electrolyte disturbances, sinusoidal waves are recorded instead of the typical form of P and QRS. If no help is provided at this stage, then a complete blockade of impulses or ventricular fibrillation develops, followed by asystole (cardiac arrest).

It should be noted that rhythm disturbances do not have a direct dependence on the content of potassium in the blood, and their severity depends on the initial electrical stability of the myocardium. In patients with angina pectoris, cardiosclerosis or myocarditis, excess potassium has a more pronounced cardiotoxic effect.

Other diagnostic methods

First of all, when examining blood, it is necessary to exclude a false increase in potassium. It is associated with its release from the cells during sampling. This situation can occur with prolonged or intense squeezing of the hand with a tourniquet, hemolysis or a high concentration of leukocytes, platelets. When blood coagulates, potassium also passes into the extracellular space, which leads to an increase in its level.

In order to correctly diagnose, you need:

• measure plasma concentration, not serum;
• explore others;
• take into account diuresis, renal filtration rate;
• exclude the influence of medicines and food;
• analyze the gas and acid-base composition of the blood;
• determine the activity of renin and aldosterone in the blood.

Treatment of hyperkalemia

A slight increase (up to 5.5 mmol / l) with preserved kidney function does not require special treatment. If signs of arrhythmia appear, or the patient has renal insufficiency, then therapy begins from the first minutes of diagnosis. The purpose of therapeutic measures is to transfer potassium into the cells and accelerate its removal from the body, restoring a normal ECG.

Correction in children

If potassium is in the range up to 7 mmol/l, then the introduction of a cation exchange resin (sodium polystyrene sulfonate with sorbitol) is usually sufficient.

At higher values ​​and changes in the electrocardiogram, calcium gluconate and sodium bicarbonate are administered. If this was not enough, then a dropper with glucose and short-acting insulin is connected. All this time, it is necessary to monitor the electrolyte composition of the blood and ECG. In severe condition, hemodialysis is performed.

Adult drugs

The main medicines can be used the same as for children, but in appropriate dosages. If necessary, beta-agonists are added to therapy, which reduce the level of potassium (Ventolin, Salbutamol) and diuretics (Lasix, Hypothiazide), which accelerate its excretion in the urine.

With a deficiency of aldosterone, it is required to provide its injection (Desoxycorticosterone acetate).

Diet for acute hyperkalemia

Foods rich in potassium are completely excluded from the diet. To do this, you need to follow these recommendations:

• vegetables - all fresh are prohibited, only boiled, greens, avocados, lentils, beans, green peas, potatoes are not recommended;
• fruits - a lot of potassium in bananas, melons, watermelon, citrus fruits, plums, apricots, grapes, cherries, pineapple, any dried fruits, so they are not allowed to patients;
• you can not eat meat, fish, you can not exceed 100 g of boiled chicken liver or shrimp per day;
• rye and bran bread, buckwheat, soy, chocolate, cocoa, molasses, nuts (especially peanuts) are removed from the menu.

Prevention measures

It is possible to prevent hyperkalemia when conducting blood tests for electrolytes when taking potassium-sparing diuretics, beta-blockers, ACE inhibitors, and when using them, avoid adverse combinations - potassium preparations in tablets, vitamin complexes, dietary supplements or table salt substitutes.

If long-term therapy with drugs that affect the concentration of potassium is planned, then a prerequisite is to monitor the filtration capacity of the kidneys and adjust the dose when it is reduced. It is also important to monitor the main functions of the myocardium using an ECG.

Hyperkalemia occurs when potassium is retained in the body due to impaired kidney function or massive cell destruction. It is characterized by muscle weakness, heart rhythm disturbance. In severe cases, ascending paralysis and cardiac arrest are possible.

For diagnosis, a blood test is performed and typical changes in the ECG are detected. A slight deviation can be corrected by diet, and if clinical or ECG signs appear, urgent therapy is necessary. With the ineffectiveness of medications, hemodialysis is prescribed.

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Electrolyte imbalance in the body leads to many disorders. Hyperkalemia is a condition in which the patient's blood contains an increased content of potassium salts (a concentration of more than 5 mmol / l). Most often, this pathology is associated with metabolic disorders. Potassium enters the body with food and is excreted by the kidneys. Hyperkalemia is possible either with the artificial formation of an excessive amount of this ion, or with functional disorders of the kidneys.

The reasons

In general, the mechanism of increasing the level of potassium in the blood is associated with impaired release of this chemical element from the cells or the pathology of its excretion by the kidneys. Improper nutrition rarely becomes the real cause of the disease, as the body is able to adapt to the diet and strengthen the excretion mechanisms. Iatrogenic (that is, caused by an incorrect treatment regimen) hyperkalemia most often occurs in patients with chronic renal failure. Usually the cause of the imbalance is excessive parenteral administration of potassium.

There is also pseudohyperkalemia. It may be due to irregularities in the technique of blood sampling (for example, when a nurse tied a tourniquet for a long time), the destruction of red blood cells, an increase in the level of platelets or white blood cells. In fact, pseudohyperkalemia is a consequence of the release of potassium from the cells during blood sampling. Such an imbalance is “false”, since, in general, the level of potassium in the body is within the normal range, and only analysis gives increased results.

It is possible to suspect pseudohyperkalemia when the patient has no signs of a pathological condition and there are no logical reasons for its occurrence. Physiological hyperkalemia can be caused by increased physical activity and injury. It should be noted that usually following this condition, hypokalemia develops, that is, a lack of potassium. In general, the causes of hyperkalemia are:

Symptoms

Regardless of the etiology of the pathological condition, in the early stages, hyperkalemia is asymptomatic. Often, the disease is detected when diagnosing other pathologies, in particular during an ECG. In such cases, the only sign of imbalance is a change in the rhythm of the heart, but for the patient himself this goes unnoticed. As the concentration of potassium in the blood increases, the number of symptoms increases. A dangerous condition becomes noticeable only when cardiotoxicity occurs. The main signs of hyperkalemia:

• A decrease in the frequency of urination due to a decrease in the number of urges - leads to a decrease in the volume of fluid excreted by the body.
• Unexpected causeless vomiting, nausea, lack of appetite.
• Stomach pains of varying severity.
• Weakness and fatigue.
• Sensation of irregular heart rhythm (feeling of “failures” in the work of the heart, “thumps” in the chest; occasional feeling that the heart stops or freezes).
• Convulsive attacks.
• Swelling of the legs.
• Frequent fainting.
• Decreased sensitivity, the appearance of a tingling sensation in the legs and lips.
• Progressive paralysis, which in some cases can be quite dangerous (if it affects the respiratory system).
• Apathy and detachment.

The main manifestations of an imbalance of potassium in the blood are muscle weakness, atony (a decrease in the number of contractions and loss of tone) of the intestine, muscle paralysis and pain, cardiac arrhythmias, and a decrease in the number of heart contractions (bradycardia). With hyperkalemia in children, the same symptoms are usually observed. Other childhood manifestations of hyperkalemia include lethargy, low mobility, mild muscle paralysis, bradycardia, and hypotension (low blood pressure).

Treatment

In the first stages of the disease, when the concentration of potassium in the plasma is 5-6 meq / l, and there are no changes in the ECG, a rather weak therapeutic effect. Patients are prescribed a hypokalemia diet and taking loop-acting diuretics. If the patient is taking drugs that may affect potassium levels, they should be discontinued. Quite often, sodium polystyrene sulfonate, previously dissolved in sorbitol, is prescribed. This substance can bind and remove excess trace element through the intestinal mucus. The drug is prescribed either inside or in the form of enemas. This method of treatment is especially effective for children and patients with gastrointestinal diseases.

With severe hyperkalemia, when the potassium concentration exceeds 6 mmol / l, and characteristic changes are noticeable on the ECG, urgent therapy is required. It should be aimed at moving the trace element inside the cells. To achieve this effect, most patients are prescribed droppers with a solution of calcium gluconate. It reduces the negative impact of potassium on the heart muscle.

This method should be used with caution in the treatment of patients taking cardiac glycosides. The effect of therapy is immediate (within a few minutes), but it will only last for a short time. Taking insulin and albuterol gives the desired result a little later (after about 1-1.5 hours), but the result is also short-lived. To remove excess potassium in severe conditions, polystyrene sulfonate is also used. In case of renal insufficiency, all these measures will not be enough, hemodialysis is necessary.

Diet for patients with hyperkalemia

To reduce the amount of potassium consumed with food to the recommended norms of 40-60 mmol per day, patients are advised to adhere to a certain diet. It is recommended to exclude or limit the consumption of dairy products, fish, some vegetables and products from them (beets, tomatoes, tomato pastes or sauces), bran, chocolate (in any form), watermelons, linseed oil, soy products, dried fruits, nuts and seeds. In addition, fast food and fast packaged meals are banned. Most often, potassium chloride is added instead of salt.

It is better to replace forbidden dishes and foods with those that reduce the amount of potassium in the blood. To do this, add more carrots, cabbage, greens, citrus fruits, berries and fruits to the diet. The concentration of the trace element is positively affected by pasta and rice. It is recommended to add alfalfa sprouts to vegetable or fruit salads.

Hyperkalemia is a serious and sometimes emergency condition. An electrolytic imbalance requires prompt, qualified assistance from a medical specialist. If you have a mild stage of pathology, do not delay the treatment and clearly follow all the recommendations of your doctor. Remember that the result of the measures taken depends only on your involvement in the therapy process and on your desire to be cured!

Hyperkalemia is a symptom that reflects disorders of electrolyte homeostasis. However, in conditions of increasing renal failure, hyperkalemia can turn into a formidable complication that can lead to death when progressing.

Timely identification of the causes of hyperkalemia and the initial stages of its treatment should be carried out by a doctor of any specialty, followed by the involvement of specialists in the profile of the underlying disease and / or specific methods of treatment, for example, extracorporeal hemocorrection.

Normally, the concentration of extracellular potassium is in the range of 3.5-5.0 mmol/L. Laboratory indicators for the determination of potassium in the blood serum may vary slightly depending on the population of the population and the accuracy of the method for determining potassium.

From the standpoint of pathophysiology, hyperkalemia is divided into 3 categories according to severity:

• mild (5.5-6.0 mmol/l);
• moderate (6.1-6.9 mmol/l);
• severe (>7.0 mmol/l).

In recent decades, the clinical approach to assessing hyperkalemia and its division into two degrees of severity has become the leading one:

• life-threatening hyperkalemia (> 6.5 mmol / l and / or the presence of ECG signs characteristic of hyperkalemia);
• non-life-threatening hyperkalemia<6,5 ммоль/л и отсутствие ЭКГ-признаков, характерных для гиперкалиемии).

Clinical manifestations of hyperkalemia

Hyperkalemia changes the functional excitability of tissues, reducing the ratio between intracellular and extracellular potassium content. The most vulnerable organ is the heart. Severe hyperkalemia can cause a slowdown in the conduction of excitation through the myocardium up to its complete stop.

It should be noted that there was a low correlation between the level of potassium in the blood and changes in the electrocardiogram (ECG), as well as the degree of their severity. According to the clinical data of R. Ahee and A. V. Crowe, only in 62% of cases hyperkalemia over 6.5 mmol/l was accompanied by ECG changes.

Of great importance is the rate of development of hyperkalemia. Thus, patients with chronic renal failure and persistent hyperkalemia may not have disturbances in the electrical activity of the heart, while a patient with deregulated diabetes mellitus and a sudden lack of insulin, which ensures the flow of glucose and potassium into the cell, can quickly show signs of hyperkalemia on the ECG.

Nerve conduction disorders. Nerve conduction disorders due to hyperkalemia may present with neurological symptoms (tingling, paresthesia). With an increase in plasma potassium of more than 8 mmol / l, generalized muscle weakness, ascending paralysis may be noted.

Disorders of the central nervous system and gastrointestinal tract. They are detected extremely rarely and are nonspecific (irritability, anxiety, abdominal cramps, diarrhea).

Conduction disorders of electrical excitation in the myocardium. ECG recorded deviations in myocardial activity as hyperkalemia increases usually progress in the following sequence:

• an increase in the T wave (potassium 6-7 mmol / l);
• expansion or absence of the P wave, expansion of the QRS complex (potassium 7-8 mmol / l);
• sinusoidal QRST (potassium 8-9 mmol/l);
• atrioventricular blockade, ventricular tachycardia/fibrillation (potassium >9 mmol/l).

Diagnosis of hyperkalemia

I stage

1. Rule out erroneous hyperkalemia:

• laboratory error;
• hemolysis;
• hemolytic anemia;
• leukocytosis more than 70x109/l;
• platelets more than 1000x109 / l.

It is urgent to re-determine the level of potassium in the blood, as well as to examine the acid-base state of the blood.

1. Assess hyperkalemic myocardial conduction disorders.

It is urgent to perform an ECG to assess the state of hyperkalemia and the need for urgent treatment.

II stage

Find out the cause / combination of causes / hyperkalemia, based on the following logical chain:

• increased intake
• redistribution inside-outside cells
• separation violation.

Increased intake potassium into blood:

• with food/enteral nutrition;
• with infusion media;
• with massive tissue destruction:
• hemolysis in internal cavities;
• large hematomas;
• positional compression syndrome;
• crash syndrome;
• posthypoxic reperfusion.

Potassium redistribution between cells and extracellular fluid:

• acidosis;
• hypoxia;
• hyperthermia;
• intracellular dehydration;
• convulsions;
• side effects of beta-blockers;
• hyperosmolarity.

Impaired excretion of potassium from the body:

• chronic renal failure (determination of glomerular filtration rate, creatinine and blood urea levels);
• acute kidney damage - oliguria, anuria (determination of hourly diuresis, creatinine and blood urea levels);
• direct action of drugs (the use of potassium-sparing diuretics);
• decrease in the concentration or activity of aldosterone:
• Addison's disease;
• hereditary defect of C21-hydroxylase;
• tubular acidosis type VI;
• hyporenic aldosteronism (determination of the concentration of renin and aldosterone in the blood);
• side effects of drugs (heparin, prostaglandin inhibitors, angiotensin-converting enzyme inhibitors, spironolactone, cyclosporine);
• violation of potassium secretion in the distal nephron (congenital or acquired).

Renal failure with a significant decrease in daily diuresis is the most common cause of hyperkalemia.

In cases of preserved volume of urine excreted and there are difficulties in finding out the cause of hyperkalemia, it is advisable to assess the level of potassium excretion by the kidneys. To do this, it is necessary to measure the level of osmolarity and the level of potassium in the urine and blood serum, and then calculate the transtubular potassium gradient (THC) using the following formula:

A THC value greater than 7 suggests normal aldosterone function and an intact tubular mechanism for potassium excretion. THC less than 7 indicates secondary disorders of potassium secretion by the tubules due to aldosteronism.

Treatment of life-threatening hyperkalemia

Life-threatening hyperkalemia with a plasma potassium level of more than 6.5 mmol / l and / or the presence of ECG changes characteristic of hyperkalemia is a clinical condition that requires urgent correction of potassium levels. The patient should be admitted to the ICU/ICU and connected to a heart monitor.

Serum potassium should be retested and erroneous hyperkalemia ruled out.

If the fact of intravenous administration of potassium-containing drugs is detected, a repeated blood test for potassium should be performed no earlier than 30 minutes after stopping their infusion.

Emergency treatment should be directed to:

• elimination of the cause of hyperkalemia (acute urinary retention, inadequate artificial ventilation of the lungs, hyperthermia, convulsions);
• discontinuation of the administration of medicines containing potassium, and / or restriction of foods rich in potassium;
• the abolition of drugs that contribute to the aggravation of hyperkalemia (beta-blockers, non-specific anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, arginine, spironolactone, cyclosporine, cellular components of canned blood);
• stabilization of the state of cardiomyocyte membranes to counteract rhythm disturbances;
• the movement of potassium from the extracellular space into the cells;
• activation of the excretion of potassium from the body.

Stabilization of the state of cardiomyocyte membranes

The introduction of calcium ions in order to stabilize the state of cardiomyocyte membranes should be carried out in the presence of ECG changes characteristic of hyperkalemia, or difficult to interpret ECG changes.

Calcium preparations are administered intravenously (with a 10 ml syringe of 10% calcium gluconate solution 2-4 times slowly with intervals between injections of 5-10 minutes). This component of treatment does not affect the level of potassium in the blood. The effect of intravenous administration of calcium occurs after a few minutes and lasts 0.5-1.0 hours. The effect of calcium action is estimated by the dynamics of the ECG pattern.

In the absence of calcium gluconate, calcium chloride can be used in 3 ml of a 10% solution, given that in each gram of calcium gluconate there are 3 times less calcium ions (4.5 meq) than in a gram of calcium chloride (13.6 meq).

For patients treated with digitalis preparations, calcium preparations should be administered slowly, over 20-30 minutes, after diluting in 100 ml of 5% glucose solution.

The movement of potassium from the extracellular space into the cell

Insulin administration. Intravenous 10-12 units of insulin and 40-60 g (100-150 ml 40%, 250-500 ml 10%) glucose. If, as a result of treatment, the blood glucose level exceeds 10 mmol / l, then additional insulin should be administered at the rate of 0.05 U / kg per hour.

Insulin binds to specific receptors and, through a certain messenger, stimulates the action of the Na + -K + pump in the direction of moving potassium into the cells. This effect of insulin is distinct from its effect on glycemia.

The action of glucose with insulin develops within 15 minutes and lasts up to 6 hours. The maximum effect of insulin can be expected after 1 hour from the start of treatment in the form of a decrease in hyperkalemia by 0.5-1.0 mmol / l.

Administration of beta agonists. Intravenous salbutamol (albuterol) 0.5 mg or inhalation 10-20 mg in a nebulizer. Salbutamol binds to β2 receptors in the liver and muscles, which leads to the conversion of ATP to 3'5'AMP. The latter, in turn, stimulates the Na + -K + pump in the direction of moving potassium into the cells.

The action of the drug with both methods of administration begins in the region of half an hour. The peak of action with intravenous administration is noted after 1 hour, and with the introduction through a nebulizer - after an hour and a half from the start of use. Intravenous administration of 0.5 mg of salbutamol can lower the level of potassium in plasma by 0.8-1.4 mmol / l, inhalation administration through a nebulizer - by 0.5-1.0 mmol / l.

Tachycardia and tremor are more pronounced with intravenous administration of salbutamol. And therefore, in the presence of coronary heart disease, the administration of the drug through a nebulizer is preferable. The effect of the action of beta-agonists is largely leveled against the background of the simultaneous use of beta-blockers.

No clear advantage in the action of insulin or beta-agonists has been identified. Different mechanisms of action of drugs cause a synergistic effect, therefore, for a more efficient movement of potassium from the extracellular space into the cells, the combined use of a glucose-insulin mixture and beta-agonists is recommended.

Acidosis correction. Acidosis is characterized by the presence in the extracellular space of an excess amount of hydrogen ions, which make it difficult for the Na + -K + pump to move potassium into the cell.

The maximum clinical effect is expected in the presence of decompensated metabolic acidosis with a blood pH level of 7.20 or less. The concentration of potassium in the blood plasma can decrease by 0.6 mmol / l with an increase in pH by 0.1 units and vice versa.

In case of respiratory acidosis, ventilation parameters should be changed. With metabolic acidosis, intravenous administration of sodium bicarbonate solutions should be used.

To prevent hyperkalemia and acute renal failure associated with massive destruction of muscle tissue and / or their prolonged ischemia, alkalization of the blood by administering soda solutions should be done as early as possible, without waiting for the increase and decompensation of acidosis. Intravenous administration of 300-400 ml of 3% sodium bicarbonate promotes alkalinization of urine and counteracts the development of acute tubular necrosis. Further correction of blood plasma pH is carried out in accordance with the dynamics of the acid-base state.

Potential risks with the use of sodium bicarbonate include hypernatremia, fluid overload, tetany in patients with chronic renal failure, and hypocalcemia.

The introduction of sodium bicarbonate in conditions of severe hyperkalemia and severe metabolic acidosis increases the effectiveness of insulin and beta-agonists.

Activation of potassium excretion from the body

Elimination of hypovolemia(in conditions of hypovolemia, the retention of fluid removed by the kidneys, and, accordingly, potassium is protective).

Correction of hypotension sympathomimetics in conditions of normovolemia (a decrease in systolic blood pressure less than 90 mm Hg leads to a decrease in the volume of urine output and, accordingly, potassium).

Stimulation of potassium excretion in the urine with the help of loop diuretics - in patients with preserved renal function to remove fluid. The use of furosemide (40-80 mg intravenously) in combination with isotonic sodium chloride solution blocks the reabsorption of water and sodium in the ascending limb of the loop of Henle. As a result, the volume of water and sodium passing through the distal tubules increases. Increased sodium reabsorption in the distal tubules is compensated by potassium secretion.

Stimulation of potassium excretion by the intestines:

• increased peristalsis (prozerin);
• the introduction of osmotic laxatives (sorbitol 100 ml of a 20% solution);
• enterosorption with cation exchange resins.

Enterosorbent kayexalate is able to bind potassium ions in exchange for the release of sodium ions. A decrease in the level of potassium in the blood develops a few hours after the introduction of the sorbent into the gastrointestinal tract. The effect develops faster when injected into the rectum than when injected into a gastric tube or per os. A single injection of 30 g of the sorbent can reduce the level of potassium in the blood by 1 mmol/l. An increase in sodium levels, a tendency to constipation, a decrease in magnesium levels are the main side effects of kayexalate.

Performing hemodialysis. The impossibility of eliminating the cause of hyperkalemia, combined with the absence of a positive effect from the ongoing emergency treatment and the persistence of a life-threatening condition, form indications for the urgent implementation of renal replacement therapy procedures.

Long-term oligoanuria is an unfavorable background that reduces the effectiveness of conservative treatment of severe hyperkalemia and increases the frequency of hemodialysis.

The most rapid removal of potassium from the body is ensured by using hemodialysis. During blood perfusion, diffusion of potassium ions from the plasma through the membrane into the dialysate occurs due to the difference in concentrations on both sides of the membrane. The higher the initial hyperkalemia, the faster this process goes.

The level of potassium in the blood usually decreases during the first hour of hemodialysis by 1 mmol / l, over the next 2 hours - by another 1 mmol / l. Further, with the continuation of hemodialysis, the level of plasma potassium changes insignificantly.

Improvement of the patient's condition and cessation of the life-threatening level of hyperkalemia suggests further planned further clarifying diagnostic procedures and conservative treatment.

Treatment of non-life-threatening hyperkalemia

Non-life-threatening mild-to-moderate hyperkalemia refers to hyperkalemia with plasma potassium levels up to and including 6.5 mmol/l and no ECG signs of hyperkalemia. The stay of these patients is possible in wards of any type.

Treatment of non-life-threatening hyperkalemia is usually divided into short-term, aimed at eliminating the cause caused by the underlying disease, and a rapid decrease in potassium levels in order to prevent the development of life-threatening hyperkalemia, and long-term.

Directions for short-term treatment are the same as for life-threatening hyperkalemia, except that there is no need for stabilization of cardiomyocyte membranes. Emergency blood cleansing is not performed. The intensity of long-term treatment depends on the level of potassium in the blood and begins with dietary adjustments.

M.I. Gromov, A.V. Fedorov, M.A. Mikhalchuk, O.E. Zaev

Hyperkalemia is quite frequent diagnosis. Most patients have a mild form of the disease (which is generally well tolerated). Any pathogen that provokes even a moderate form of the disease must be quickly identified and eliminated in order to prevent progression to a more severe form. Severe hyperkalemia can lead to cardiac arrest and death.

A diagnosis of hyperkalemia means that the patient has an abnormally high .

Potassium contributes to the normal functioning of the nervous system and heart. It regulates the activity of smooth and skeletal muscles. Potassium is important for the transmission of electrical signals through the nervous system. Optimal potassium levels support a normal heart rhythm. The development of hypo- or hyperkalemia can lead to an abnormal heart rhythm.

The mild form of the disease has a limited effect on the heart, but mild hyperkalemia can cause changes in the ECG, and a severe form disrupts the heart rhythm, which usually leads to cardiac arrest.

Another important effect of the disease is interference with the functioning of skeletal muscles. Hyperkalemic periodic paralysis is a rare hereditary disorder in which patients have a characteristic increase in potassium levels, causing muscle paralysis.

Brief information about the disease in a visual form you can get from the video

Ask your question to the doctor of clinical laboratory diagnostics

Anna Poniaeva. She graduated from the Nizhny Novgorod Medical Academy (2007-2014) and residency in clinical laboratory diagnostics (2014-2016).

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