Description:

Hyperkalemia is a condition in which the plasma potassium concentration exceeds 5 mmol/l. It occurs as a result of the release of potassium from the cells or a violation of the excretion of potassium by the kidneys.

Abnormal potassium levels are quickly signaled by ECG changes in lead II. With hyperkalemia, pointed T-waves are observed, and with flattened T-waves and U waves.

Symptoms:

The resting potential is determined by the ratio of potassium concentrations inside the cell and in the extracellular fluid. With hyperkalemia, due to cell depolarization and a decrease in cell excitability, muscle weakness occurs, up to paresis and respiratory failure. In addition, ammoniogenesis is inhibited, the reabsorption of the ammonium ion in the thick segment of the ascending loop of Henle and, consequently, the excretion of hydrogen ions. The resulting aggravates hyperkalemia, as it stimulates the release of potassium from the cells.

The most serious manifestations are due to the cardiotoxic effect of potassium. First, high, pointed T waves appear. In more severe cases, the PQ interval lengthens and the QRS complex widens, AV conduction slows down, and the P wave disappears. The expansion of the QRS complex and its fusion with the T wave leads to the formation of a sinusoid-like curve. In the future, ventricular fibrillation and. In general, however, the severity of the cardiotoxic effect does not correspond to the degree of hyperkalemia.

Causes of occurrence:

Hyperkalemia occurs as a result of the release of potassium from cells or impaired excretion of potassium by the kidneys. Increasing potassium intake is rarely the sole cause of hyperkalemia, as potassium excretion rapidly increases through adaptive 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 sampling. It is observed in violation of the technique of venipuncture (if the tourniquet is tightened too long), hemolysis, leukocytosis, thrombocytosis. In the last two cases, potassium leaves the cells during the formation of a blood clot. Pseudohyperkalemia should be suspected if the patient does not have clinical manifestations of hyperkalemia and there are no reasons for its development. At the same time, in correctly taken blood and measuring the concentration of potassium in plasma, and not in serum, this concentration should be normal.

Potassium release from cells is observed during hemolysis, tumor decay syndrome, rhabdomyolysis, metabolic acidosis due to intracellular uptake of hydrogen ions (except for cases of accumulation of organic anions), insulin deficiency and plasma hyperosmolality (for example, with), treatment with beta-blockers (occurs rarely, but may contribute to hyperkalemia due to other factors), the use of depolarizing muscle relaxants, such as suxamethonium chloride (especially in trauma, burns, neuromuscular diseases).

Physical activity causes transient hyperkalemia, which may be followed by hypokalemia.

A rare cause of hyperkalemia is familial hyperkalemic periodic. 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 attacks of muscle weakness or paralysis that occur in situations that promote the development of hyperkalemia (for example, during exercise).

Hyperkalemia is also observed in severe due to suppression of the activity of Na +, K + -ATPase.

Chronic hyperkalemia is almost always due to a decrease in the excretion of potassium by the kidneys as a result of either a violation of the mechanisms of its secretion, or a decrease in the flow of fluid into the distal nephron. The latter reason rarely independently leads to hyperkalemia, but can contribute to its development in patients with protein deficiency (due to reduced urea excretion) and hypovolemia (due to reduced intake of sodium and chloride ions in the distal nephron).

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 chloride ions. Both of these lead to a decrease in the transepithelial potential in the cortical region of the collecting ducts.

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 the hyperkalemia that often occurs in the treatment of pneumocystis in patients with AIDS.

Hyperkalemia is often observed in oliguric acute renal failure due to an increase in the release of potassium from cells (due to acidosis and increased catabolism) and a violation of its excretion.

With chronic renal failure, an increase in the flow of fluid into the distal nephron compensates for a decrease in the number of nephrons up to a certain time. However, when GFR falls below 10.15 ml/min, hyperkalemia occurs.

Hyperkalemia is often caused by an undiagnosed urinary tract obstruction.

Treatment:

For treatment appoint:

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 when the plasma potassium concentration exceeds 7.5 mmol/L. In this case, pronounced muscle weakness, the disappearance of the P wave, the expansion of the QRS complex, ventricular.

Emergency care is indicated for severe hyperkalemia. Its purpose is to recreate the normal resting potential, move potassium into the cells and increase potassium excretion. They stop the intake of potassium from the outside, cancel drugs that violate its excretion. To reduce myocardial excitability, calcium gluconate is administered, 10 ml of a 10% intravenous solution 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 in the ECG persist, the drug is administered again at the same dose.

Insulin promotes the movement of potassium into cells and a temporary decrease in its concentration in plasma. Inject 10-20 units of short-acting insulin and 25-50 g of glucose (for warning; do not administer glucose in case of 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 the concentration of potassium, although not so fast, is also observed with the introduction of only glucose (due to the secretion of endogenous insulin).

Sodium bicarbonate also helps move potassium into cells. It is prescribed for severe hyperkalemia with metabolic acidosis. The drug should be administered as an isotonic solution (134 mmol/l). For this, 3 ampoules of bicarbonate are diluted in 1000 ml of 5% glucose. In CKD, sodium bicarbonate is ineffective and can lead to sodium overload and hypervolemia.

Beta2-adrenergic stimulants, when administered parenterally or inhaled, also promote the movement of potassium into cells. The action begins after 30 minutes and lasts 2-4 hours. Plasma potassium concentration decreases by 0.5-1.5 mmol / l.

Diuretics, cation exchange resins and hemodialysis are also used. With normal renal function, loop and thiazide diuretics, as well as their combination, increase the excretion of potassium. Cation-exchange resin sodium polystyrenesulfonate exchanges potassium for sodium in the gastrointestinal tract: 1 g of the drug binds 1 mmol of potassium, as a result, 2-3 mmol of sodium is released. The drug is administered orally at a dose of 20-50 g in 100 ml of a 20% sorbitol solution (for warning). The action occurs after 1-2 hours and lasts 4-6 hours. Plasma potassium concentration decreases by 0.5-1 mmol / l. Sodium polystyrene sulfonate can be administered as an enema (50 g of the drug, 50 ml of a 70% sorbitol solution, 150 ml of water).

Sorbitol is contraindicated in the postoperative period, especially after kidney transplantation, as it increases the risk of colon.
- the fastest and most effective way to reduce the concentration of potassium in plasma. It is indicated in case of severe hyperkalemia with the ineffectiveness of other conservative measures, as well as in patients with acute renal failure and chronic renal failure. To reduce the concentration of potassium in the plasma can be used, however, in terms of efficiency, it is significantly inferior to hemodialysis. Be sure to carry out treatment aimed at eliminating the cause of hyperkalemia. It includes diet, elimination of metabolic acidosis, increase in extracellular fluid volume, administration of mineralocorticoids.

Content

After undergoing a comprehensive medical examination, patients may find out that they have an increased amount of potassium in the blood. A mild form of the violation is not dangerous to human health. If left untreated, the pathology progresses and can provoke a cardiac arrest in the patient. To prevent the negative consequences of the disease, it is recommended to study in detail its features, signs and causes.

What is hyperkalemia

Potassium is the best known intracellular cation. The element is excreted from the body through the urinary tract, sweat glands, and the gastrointestinal tract. In the kidneys, excretion can be passive (glomeruli) or active (proximal tubules, ascending loop of Henle). Transportation is provided by aldosterone, the synthesis of which is activated by the hormone renin.

Hyperkalemia is an increase in the concentration of potassium in the patient's blood plasma. The disease causes an excessive intake of the element into the body or a violation of its secretion by nephrons in the cortical section of the collecting ducts. Pathology is considered to be an increase in the level above 5 mmol / l. The condition has a code in the International Classification of Diseases (ICD-10) - E 87.5. The concentration of potassium at the level of 3.5-5 mmol / l is considered the norm. A significant increase in indicators leads to a violation of the heart rhythm and requires emergency care.

Causes

The disease develops after the redistribution of potassium from the cells into the blood and the delay in the filtration of this element by the kidneys. In addition, there are other causes of hyperkalemia:

• diabetes;
• kidney failure;
• lupus erythematosus;
• nephropathic disorders;
• violation of the structure of the renal tissue;
• destruction of blood cells (erythrocytes, platelets, leukocytes);
• abuse of nicotine, alcohol, drugs;
• lack of oxygen;
• abuse of drugs or foods high in potassium;
• congenital anomalies in the structure or functioning of the kidneys;
• diseases that cause the breakdown of glycogen, peptides, proteins;
• insufficient excretion of potassium along with urine;
• autoimmune diseases;
• mineralocorticoid deficiency.

Symptoms

Regardless of the cause of the development of pathology, in the early stages, the symptoms of hyperkalemia are difficult to notice. The disease may not manifest itself for a long time. Often, doctors begin to suspect its presence during the diagnosis of other problems using an ECG. The first conduction disturbances, confirming the presence of hyperkalemia in a person, may proceed unnoticed. With the progression of the pathology, the number of symptoms increases. It is worth starting treatment if the following are found signs of illness:

• convulsions;
• apathy;
• swelling of the lower extremities;
• sudden fainting;
• muscle weakness;
• labored breathing;
• numbness of the limbs;
• decreased urge to urinate;
• pain in the stomach of varying intensity;
• sudden vomiting;
• increased fatigue;
• general weakness;
• an uncomfortable tingling sensation on the lips;
• progressive paralysis.

Hyperkalemia on ECG

This pathology provokes neuromuscular disorders and problems with the cardiovascular system. Myocardial contractility after the onset of the disease does not suffer, but conduction changes lead to severe arrhythmias. According to the ECG, signs of hyperkalemia can be seen if the concentration of potassium in the blood exceeded 7 mmol / l. A moderate increase in the level of this element is indicated by a high pointed T wave with a normal QT interval. The amplitude of the P wave decreases, and the PQ interval lengthens.

As the pathology progresses, atrial asystole appears, the QRS complexes expand, and a sinusoidal curve may appear. This indicates fibrillation (chaotic contraction) of the ventricles. If the concentration of potassium exceeds 10 mmol / l, the patient's heart stops in systole (at the time of contraction without further relaxation), which is typical only for this disease.

The effect of pathology on the heart is enhanced by acidosis (increased acidity), hyponatremia, hypocalcemia (decrease in the level of sodium and calcium in the blood serum). At a potassium concentration above 8 mmol / l, the patient has a decrease in the rate of propagation of excitation along the nerves, muscle strength in the limbs, and respiratory disorders are noted.

ECG results are directly correlated with potassium balance. A dangerous change in the heart rhythm at any stage of the development of hyperkalemia becomes noticeable to the patient. If a patient is diagnosed with heart pathologies, then the only sign of this disease, detected by an electrocardiogram, may be bradycardia. It is worth noting that changes in the human ECG represent a sequential progression, which, with an increase in the concentration of potassium in the blood, correlates (corresponds) only approximately.

As the disease progresses, the level of the chemical element may increase. Depending on the stage of the pathology, during the study, the following indicators can be obtained:

1. 5.5-6.5 mmol/l: ST-segment depression, short QT interval, tall and narrow T-waves.
2. 6.5-8 mmol / l: the P-R interval is extended, peaked T-waves, the P wave is absent or reduced in size; The QRS complex is enlarged.
3. More than 8 mmol / l: P wave is absent, ventricular rhythm, QRS complex is increased.

Diagnostics

At the initial stage of research, it is important to clarify the time of appearance of the first symptoms of the disorder and the causes. In addition, specialists must make sure that the patient has not taken any medications that can affect the level of potassium in the blood. The main sign of pathology is a change in heart rate, therefore, with an ECG, a specialist may suspect the presence of a disease.

Although the results of the electrocardiogram are informative, specialists may order a number of additional studies for the patient, including general tests. To accurately diagnose and determine the stage of the disease, a blood test for electrolytes is done. Assessment of kidney function is carried out if the patient's ratio of nitrogen and creatine indicates renal failure and a change in the level of clearance of the latter. In addition, an ultrasound of this organ may be prescribed.

In each case, diagnostic measures are selected individually. Based on clinical data, the following laboratory tests may be prescribed to the patient:

• glucose level (if there is a suspicion of diabetes mellitus);
• gas composition of arterial blood (if acidosis is suspected);
• digoxin level (in the treatment of chronic circulatory failure);
• assessment of the levels of aldosterone and cortisol in the blood serum;
• urinalysis for phosphorus content (with tumor lysis syndrome);
• urine myoglobin (if blood is found in the general analysis).

Treatment of hyperkalemia

Methods of therapy for this disease are selected for each patient individually, taking into account the general condition of the body, the causes of the development of the disease and the severity of the symptoms. Mild hyperkalemia is treated without hospitalization. With serious changes in the ECG, the patient needs emergency care. Severe hyperkalemia requires intensive care in a hospital setting.

The treatment regimen is set individually for each patient. Based on clinical studies, therapy may include the following activities:

1. Diet low in potassium (for mild forms).
2. Cancellation of drugs that increase the concentration of potassium: Heparin, ACE inhibitors and others (if necessary).
3. Medical treatment.
4. Treatment of diseases that caused an increase in the concentration of an element in the blood, atrioventricular blockade.
5. Hemodialysis (purification of the blood with the help of special equipment). The procedure is prescribed in the absence of the effect of other methods of therapy.

Medical treatment

Severe and moderate stages of the disease are not complete without the use of medications. Depending on the specific case, patients are prescribed the following types of drugs:

1. Sodium bicarbonate is used in the treatment of metabolic acidosis or renal insufficiency.
2. Cation exchange resins (drugs that bind potassium and remove it through the gastrointestinal tract) are administered intravenously or as an enema in the rectum.
3. Intravenous solutions of chloride or calcium gluconate (10%) are used to reduce the negative impact of the disease on the heart.
4. Iron preparations are prescribed to patients with the development of anemia.
5. Insulin with dextrose - intravenously for 30 minutes to excrete potassium back into the cells.
6. Sodium bicarbonate injections to counteract acidosis (increased acidity).
7. Aldosterone (fludrocortisone or deoxycortone) is given to increase the secretion of potassium by the kidneys.
8. Veltassa - suspension for lowering the level of potassium in the blood.
9. Diuretics (Furosemide, Bumetanide, Cortineff and others) are used after the acute phase of the disease to remove excess potassium through the urinary tract.
10. Polystyrene sulfonate in enemas or orally to remove excess potassium.
11. Preparations for stimulation of beta-2-adrenergic receptors (Epinephrine, Albuterol).

Diet

In addition to drug treatment of this disease, it is recommended to increase physical activity and control nutrition. The diet should exclude an abundance of foods high in potassium. Patients with hyperkalemia should adhere to the following rules:

1. Eliminate allergens from the diet (soy, dairy products, corn, preservatives).
2. Eat lean meat, fish, exclude red varieties.
3. Reduce daily potassium intake to 2000-3000 mg.
4. Eliminate trans fats, alcohol, refined foods, caffeine, sweets, fried foods.
5. Reduce your intake of bananas, watermelons, tomatoes, potatoes, nuts, peaches, cabbage, eggplant, and other foods high in potassium.
6. Use healthy vegetable oils (coconut or olive) whenever possible.
7. Drink at least 1.5 liters of water daily.

Hyperkalemia is a condition that develops as a result of an increase in the content of potassium in the blood serum (while its level exceeds 5 mmol / l).

Hyperkalemia is diagnosed in approximately 1-10% of patients presenting to hospitals. However, its prevalence has increased in recent years. This is mainly due to an increase in the number of prescriptions to patients of drugs that can affect the RAAS (renin-angiotensin-aldosterone system), the main tasks of which are to maintain systemic arterial pressure and normal blood flow in vital organs (liver, heart, kidneys, brain).

Potassium and its role in the human body

Potassium is the main intracellular cation. Along with sodium, it maintains the balance of acids and alkalis in the body, normalizes the water-salt balance, has a decongestant effect, and activates many enzymes. In addition, it plays a key role in the conduction of nerve impulses and contraction of skeletal and cardiac muscles.

Potassium salts make up half of all salts contained in the body, and it is their presence that ensures the normal functioning of blood vessels, muscles, and endocrine glands. Potassium prevents the accumulation of excess sodium salts in the vessels and cells of the body and, thereby, has an anti-sclerotic effect. It helps prevent overwork, reduces the risk of chronic fatigue syndrome.

To ensure the optimal balance of potassium in the body, it is necessary that all its regulatory mechanisms function and interact as smoothly as possible. The role of the main mechanism-regulator of potassium is performed by the kidneys, and their activity, in turn, is stimulated and controlled by the hormone aldosterone secreted by the adrenal glands. Normally, even with an increased intake of potassium from food, this mechanism maintains its constant level in the blood serum. In cases where there is a violation of the regulation of potassium, and as a result of this, hyperkalemia develops, disturbances also occur in the activity of the nervous and cardiovascular systems.

The danger of hyperkalemia lies in the fact that it, causing disturbances in cardiac contractions, provokes a change in the course of electrical processes in it. The consequence of this is: intoxication of the body, arrhythmia and even cardiac arrest. Therefore, even with a mild form of hyperkalemia, treatment is required immediately, with the use of intensive care measures.

Causes of hyperkalemia

The main causes of hyperkalemia are a violation of the redistribution of potassium from the intracellular space to the extracellular space, as well as potassium retention in the body.

Hyperkalemia can develop as a result of a decrease in excretion (discharge) by the kidneys. This condition is caused by:

• Renal failure, when up to 1000 mEq of potassium is excreted by the kidneys during the day - a dose that significantly exceeds the amount of potassium that normally enters the body;
• Damage to the kidney tissue, as a result of which hyperkalemia develops even with a reduced (compared to the average indicator) potassium intake;
• Conditions in which the adrenal cortex secretes less aldosterone than is required for the normal functioning of the body (hypoaldosteronism). Such conditions are accompanied by adrenal insufficiency, as well as a decrease in the level of sensitivity of the epithelial tissue of the tubules to aldosterone, which is observed in patients with nephropathy, systemic lupus erythematosus, amyloidosis, with lesions of the renal interstitium, etc.

Hyperkalemia due to improper redistribution of intracellular potassium into the blood is provoked by:

• Various kinds of cell damage and their destruction, which may occur due to the destruction of blood cells (leukocytes, platelets, erythrocytes), with oxygen starvation, a decrease in blood supply to tissues, as well as their necrosis; with the development of a syndrome of prolonged tissue crushing, burns, an overdose of cocaine;
• Hypoglycemic disease due to increased breakdown of glycogen and enzymatic hydrolysis of proteins and peptides, as a result of which an excessive amount of potassium is released, leading to hyperkalemia;
• intracellular acidosis.

At the same time, excessive intake of potassium in the body with food or medications taken does not cause the development of persistent hyperkalemia.

Excessive consumption of potassium-containing foods can cause hyperkalemia only in those cases when, in parallel, the level of potassium excreted together with urine decreases in the body (in case of impaired renal function).

Symptoms of hyperkalemia

Regardless of the causes of hyperkalemia, the disease in the initial stages practically does not manifest itself. At this stage, it is often diagnosed absolutely by chance during tests or during the passage of an electrocardiogram. Prior to this, the only symptom of hyperkalemia may be only a slight disturbance of the normal heart rhythm, which, as a rule, goes unnoticed by patients.

As the pathological process progresses, the number of symptoms of hyperkalemia increases significantly. In this case, the disease is accompanied by:

• Spontaneous vomiting;
• stomach cramps;
• Arrhythmia;
• Reducing the number of urges to urinate, which is accompanied by a decrease in the amount of urine output;
• Increased fatigue;
• Frequent clouding of consciousness;
• General weakness;
• Convulsive twitching of muscles;
• Change in sensitivity and the appearance of a tingling sensation in the limbs (in the hands, feet) and in the lips;
• Progressive ascending paralysis affecting the respiratory system;
• ECG changes (the earliest symptom of hyperkalemia).

Treatment of hyperkalemia

The method of treating hyperkalemia directly depends on the nature of the course of the disease and the causes that provoked it.

With a critical increase in the level of potassium over 6 mmol / l, when the patient is threatened with cardiac arrest, it is required to take a set of emergency measures aimed at reducing it. So, intravenous administration of a solution of chloride or calcium gluconate should normally have a positive effect after 5 minutes. When this does not happen, the dose of the drug is administered again. The action of the solution continues for three hours, after which the procedure is repeated.

Subsequent therapy involves the appointment of drugs that inhibit the further development of hyperkalemia and the development of complications.

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 where the volume of urine output is preserved 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, previously diluted 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 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 includes 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 to stabilize 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 associated with a characteristic sequence of ECG changes. The earliest manifestation is a narrowing and sharpening in the form of a hut at the top of the T wave.
The QT interval at this stage is shortened, corresponding to a decrease in the duration of AP. Developing extracellular hyperkalemia reduces the resting membrane potential of the atria and ventricles, thereby inactivating sodium channels, which reduce Vmax and conduction velocity. The QRS complex begins to expand, and the amplitude of the P wave decreases. Prolongation of the PR interval may occur, sometimes followed by second- or third-degree AV block.

Complete disappearance of P waves may be associated with a nodal replacement rhythm or with the so-called sinoventricular conduction (with sinoventricular conduction, there is no excitability of the atrial myocardium with an intact conduction system.

In this case, the impulse from the sinus node is conducted to the ventricles through the AV connection with the formation of a pseudoventricular - without a P wave on the ECG - rhythm with narrow ventricular complexes.
This is a “latent sinus rhythm” that increases with exercise.)

In a later period development of hyperkalemia, the sinus impulse is conducted from the SA node to the AV node, but a clear P wave is not formed.
Moderate to severe hyperkalemia sometimes presents as ST elevation in the right precordial leads (V1 and V2) and mimics the ischemic injury current or pattern seen in Brugada syndrome. However, even severe hyperkalemia can have atypical or undiagnosed ECG changes.

Very pronounced hyperkalemia in the presence of some additional conditions leads to asystole, sometimes preceded by slow undulating (sinusoidal) ventricular flutter.

Triad consisting of tall, pointed T waves (as a result of hyperkalemia), elongated (as a result of hypocalcemia) and LVH (as a result of arterial hypertension), is a highly probable sign of chronic renal failure.

As a result of electrophysiological changes associated with hypokalemia, on the contrary, hyperpolarization of CMC membranes occurs and the duration of AP increases. The main ECG sign of this abnormality is ST depression with flattened T-waves and enlarged U-waves. The U-waves may exceed the amplitude of the T-waves.

Clinical T wave separation and U wave on surface ECGs may be difficult or even impossible. The visible U-wave in hypokalemia and other pathological conditions may indeed be part of the T-wave, the shape of which changes under the influence of a voltage gradient between M-cells, or mid-myocardial cells, and adjacent myocardial layers.

Prolongation of repolarization in hypokalemia as part of the acquired long QT(U) syndrome predisposes to torsades de pointes tachycardia. Hypokalemia when taking digitalis also increases the likelihood of tachyarrhythmias.

Educational video deciphering the ECG for electrolyte disorders