Why is it important to know the symptoms of hyperkalemia? Hyperkalemia Pressure during hyperkalemia

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 hyperkalemia, flattened T waves and U waves are observed.

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 decreased cell excitability, muscle weakness occurs, including paresis and respiratory failure. In addition, ammoniogenesis, the reabsorption of ammonium ions in the thick segment of the ascending loop of Henle and, consequently, the excretion of hydrogen ions, is inhibited. The resulting hyperkalemia aggravates because it stimulates the release of potassium from the cells.

The most serious manifestations are due to the cardiotoxic effects of potassium. First, tall, 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 merging with the T wave leads to the formation of a curve resembling a sinusoid. Subsequently, ventricular fibrillation and. In general, however, the severity of cardiotoxicity does not correspond to the degree of hyperkalemia.

Causes:

Hyperkalemia occurs as a result of the release of potassium from cells or impaired potassium excretion by the kidneys. Increased potassium intake is rarely the sole cause of hyperkalemia, since its excretion rapidly increases due to adaptive mechanisms.

Iatrogenic hyperkalemia occurs as a result of excessive parenteral potassium administration, especially in patients with chronic renal failure.

Pseudohyperkalemia is caused by the release of potassium from cells during blood collection. It is observed when the venipuncture technique is violated (if the tourniquet is tightened too long), hemolysis, leukocytosis, thrombocytosis. In the last two cases, potassium leaves the cells when a blood clot forms. Pseudohyperkalemia should be suspected if the patient has no clinical manifestations of hyperkalemia and there are no reasons for its development. Moreover, if blood is taken correctly and the potassium concentration is measured in plasma, and not in serum, this concentration should be normal.

The release of potassium from cells is observed with hemolysis, tumor collapse syndrome, rhabdomyolysis, metabolic acidosis due to intracellular uptake of hydrogen ions (except in 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 disease. 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 physical activity).

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

Chronic hyperkalemia is almost always caused by a decrease in potassium excretion 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 cause rarely leads to hyperkalemia on its own, but can contribute to its development in patients with protein deficiency (due to decreased urea excretion) and hypovolemia (due to reduced supply of sodium and chlorine ions to the distal nephron).

Impaired 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 lead to a decrease in transepithelial potential in the cortical collecting duct.

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 during the treatment of Pneumocystis cystica in patients with AIDS.

Hyperkalemia is often observed in oliguric acute renal failure due to increased cellular potassium release (due to acidosis and increased catabolism) and impaired potassium excretion.

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

Undiagnosed urinary tract obstruction is often the cause of hyperkalemia.

Treatment:

For treatment the following is prescribed:

Treatment depends on the degree of hyperkalemia and is determined by the plasma potassium concentration, the presence of muscle weakness, and ECG changes. Life-threatening hyperkalemia occurs when plasma potassium concentrations exceed 7.5 mmol/L. In this case, pronounced muscle weakness, disappearance of the P wave, expansion of the QRS complex, and ventricular pain are observed.

Emergency care is indicated for severe hyperkalemia. Its goal is to recreate normal resting potential, move potassium into cells and enhance potassium excretion. Stop the intake of potassium from the outside, and discontinue medications that interfere with its excretion. To reduce myocardial excitability, calcium gluconate and 10 ml of 10% solution are administered intravenously over 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 re-administered at the same dose.

Insulin promotes the movement of potassium into cells and a temporary decrease in its concentration in plasma. 10-20 units of short-acting insulin and 25-50 g of glucose are administered (for prevention; in case of hyperglycemia, glucose is not administered). The action lasts for several hours, 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 when only glucose is administered (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). To do this, 3 ampoules of bicarbonate are diluted in 1000 ml of 5% glucose. In chronic renal failure, sodium bicarbonate is ineffective and can lead to sodium overload and hypervolemia.

Beta2-agonists, when administered parenterally or inhaled, also promote the movement of potassium into 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. At normal function kidney loop and thiazide diuretics, as well as their combination, increase potassium excretion. The cation exchange resin sodium polystyrene sulfonate exchanges potassium for sodium in the gastrointestinal tract: 1 g of the drug binds 1 mmol of potassium, resulting in the release of 2-3 mmol of sodium. The drug is prescribed orally in a dose of 20-50 g in 100 ml of 20% sorbitol solution (for prevention). The effect occurs within 1-2 hours and lasts 4-6 hours. The concentration of potassium in plasma decreases by 0.5-1 mmol/l. Sodium polystyrene sulfonate can be administered as an enema (50 g of the drug, 50 ml of 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 cancer.
- the fastest and most effective way to reduce potassium concentration in plasma. It is indicated in cases of severe hyperkalemia when other conservative measures are ineffective, as well as in patients with acute renal failure and chronic renal failure. To reduce the concentration of potassium in plasma, it can be used, but it is significantly inferior in effectiveness to hemodialysis. Be sure to carry out treatment aimed at eliminating the cause of hyperkalemia. It includes diet, elimination of metabolic acidosis, increasing the volume of extracellular fluid, and the administration of mineralocorticoids.

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

Hyperkalemia is diagnosed in approximately 1-10% of patients presenting to hospitals. However, in last years its prevalence is increasing. This is mainly due to the 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 maintaining systemic blood 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. It, along with sodium, maintains the balance of acids and alkalis in the body, normalizes water-salt balance, has an anti-edematous effect, and activates many enzymes. In addition, it plays a key role in the processes 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 blood vessels and cells of the body and, thereby, has an anti-sclerotic effect. It helps prevent overwork and reduces the risk of chronic fatigue syndrome.

To ensure optimal potassium balance 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 ensures the maintenance of its constant level in the blood serum. In cases where potassium regulation is disrupted and, as a consequence, hyperkalemia develops, disturbances also occur in the activity of the nervous and cardiovascular systems.

The danger of hyperkalemia lies in the fact that, by causing disturbances in heart contractions, it 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 mild form Hyperkalemia requires immediate treatment using 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 may develop as a consequence of decreased excretion by the kidneys. This condition is provoked by:

Renal failure, when the kidneys excrete up to 1000 mEq of potassium during the day - a dose significantly higher than the amount of potassium normally entering the body;
Damage to the kidney tissue, as a result of which hyperkalemia develops even with a reduced (compared to the average) 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 tubular epithelial tissue to aldosterone, which is observed in patients with nephropathy, systemic lupus erythematosus, amyloidosis, with lesions of the renal interstitium, etc.

Hyperkalemia, caused by improper redistribution of intracellular potassium into the blood, is provoked by:

Various types of cell damage and destruction, which can occur due to the destruction of blood cells (leukocytes, platelets, red blood cells), due to oxygen starvation, decreased blood supply to tissues, as well as their necrosis; with the development of prolonged tissue crush syndrome, burns, cocaine overdose;
Hypoglycemic disease caused by increased breakdown of glycogen and enzymatic hydrolysis of proteins and peptides, resulting in the release of excessive amounts of potassium, leading to hyperkalemia;
Intracellular acidosis.

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

Excessive consumption of potassium-containing products can cause hyperkalemia only in cases where, in parallel, the level of potassium excreted in the body in the urine decreases (in case of impaired renal function).

Symptoms of hyperkalemia

Regardless of the causes of hyperkalemia, the disease practically does not manifest itself in the initial stages. At this stage, it is often diagnosed completely by accident during tests or an electrocardiogram. Before this, the only symptom of hyperkalemia may be only a slight disturbance in 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. This disease is accompanied by:

Spontaneous vomiting;
Stomach cramps;
Arrhythmia;
A decrease in the number of urges to urinate, which is accompanied by a decrease in the amount of urine excreted;
Increased fatigue;
Frequent clouding of consciousness;
General weakness;
Convulsive muscle twitching;
Changes in sensitivity and the appearance of a tingling sensation in the limbs (hands, feet) and 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 disease and the causes that provoked it.

If the potassium level increases critically above 6 mmol/l, when the patient is in danger of cardiac arrest, it is necessary to take a set of emergency measures aimed at reducing it. Thus, intravenous administration of a solution of calcium chloride or gluconate should normally have a positive effect after 5 minutes. When this does not happen, the dose of the drug is re-administered. The action of the solution lasts for three hours, after which the procedure is repeated.

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

Hyperkalemia is a condition in which the concentration of potassium electrolytes (K+) in the blood rises to life-threatening levels. A patient with hyperkalemia requires emergency medical attention due to the potential risk of cardiac arrest if not treated promptly.

The normal level of potassium in the blood ranges from 3.5 to 5.0 mEq/L, about 98% of potassium is found inside the cells, and the remaining 2% in the extracellular fluid, including the blood.

Potassium is the most abundant intracellular cation and is important for many physiological processes, including the maintenance of resting membrane potential, cell volume homeostasis, and the transmission of action potentials in nerve cells. Its main food sources are vegetables (tomatoes and potatoes), fruits (oranges and bananas) and meat. Potassium is excreted through gastrointestinal tract, kidneys and sweat glands.

Hyperkalemia occurs when there is excess intake or ineffective excretion of potassium. An increase in extracellular potassium levels leads to depolarization of the cell membrane potential due to an increase in the equilibrium potassium potential. Depolarization leads to tension of sodium channels, opens them, and also increases their inactivation, which ultimately leads to ventricular fibrillation or asystole. Prevention of recurrence of hyperkalemia usually involves reducing dietary potassium intake and potassium-sparing diuretics.

Symptoms of hyperkalemia

Symptoms of hyperkalemia are nonspecific and usually include:

Malaise;
The appearance of high T-waves on the ECG;
Ventricular tachycardia;
Muscle weakness;
Increased ORS interval on ECG;
Increased P-R interval on ECG.

Also symptoms of hyperkalemia are cardiac arrhythmia, sharpening of the T wave on the ECG and potassium levels exceeding 7.0 mmol/l.

Causes of hyperkalemia

The causes of hyperkalemia may be ineffective elimination of renal failure, Addison's disease and aldosterone deficiency. The following can also lead to hyperkalemia:

Hyperkalemia may also be caused by congenital adrenal hyperplasia, Gordon's syndrome, and type IV renal tubular acidosis.

Hyperkalemia can be caused by the use of potassium supplements, potassium chloride infusions, and excessive consumption of potassium-containing salt.

Diagnosis of hyperkalemia

To collect sufficient information to diagnose hyperkalemia, it is necessary to constantly measure potassium levels, because its elevated state may be associated with hemolysis in the first stage. Normal serum potassium levels range from 3.5 to 5 mEq/L. Typically, diagnosis includes blood tests for kidney function (creatinine, blood urea nitrogen), glucose, and sometimes creatine kinase and cortisol. Calculation of the transtubular potassium gradient is sometimes helpful in identifying the cause of hyperkalemia, and electrocardiography is performed to determine the risk of cardiac arrhythmias.

Treatment of hyperkalemia

The choice of treatment depends on the degree and cause of hyperkalemia. When the potassium level in the blood exceeds 6.5 mmol/l, it is urgent to lower the potassium level to normal levels. This can be achieved by administering calcium (calcium chloride or calcium gluconate), which increases the threshold potential and restores the normal gradient between the threshold potential and the resting membrane potential, which increases with abnormal hyperkalemia. One ampoule of calcium chloride contains approximately three times more calcium than calcium gluconate. Calcium chloride begins to work in less than five minutes, and its effect lasts about 30-60 minutes. The dosage should be adjusted while closely monitoring ECG changes during administration and the dose should be repeated if ECG changes do not normalize within 3 to 5 minutes.

Also, to treat hyperkalemia and reduce the risk of complications, it is possible to carry out certain medical procedures that help stop the process of hyperkalemia for a while until potassium is removed from the body. These include:

Intravenous administration of 10-15 units of insulin along with 50 ml of 50% dextrose solution to prevent hyperkalemia leads to the displacement of potassium ions into the cells. Its effects last for several hours, so it is sometimes necessary to take other measures at the same time to suppress potassium levels on a more permanent basis. Insulin is usually administered with an appropriate amount of glucose in order to prevent hypoglycemia after insulin administration;
Bicarbonate therapy (infusion of 1 ampoule (50 mEq) over 5 min) is effective way by the displacement of potassium into cells. Bicarbonate ions stimulate the exchange of H+ for Na+, which leads to stimulation of sodium-potassium ATPase;
Administration of salbutamol (albuterol, Ventolin), β 2-selective catecholamines 10-20 mg. This drug also reduces K+ levels, speeding up its movement into cells.

Treatment of hyperkalemia in severe forms requires hemodialysis or hemofiltration, which are the fastest methods of removing potassium from the body. They are usually used in cases where the underlying cause of hyperkalemia cannot be corrected quickly or there is no response to other measures taken.

Sodium polystyrene sulfonate with sorbitol, taken orally or rectally, is widely used to reduce potassium within a few hours, and furosemide is used to remove potassium in the urine.

Video from YouTube on the topic of the article:

What is Hyperkalemia
What causes hyperkalemia
Symptoms of Hyperkalemia
Diagnosis of Hyperkalemia
Treatment of Hyperkalemia

What is Hyperkalemia

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. Hyperkalemia produces pointed T waves, while hypokalemia produces flattened T waves and U waves.

What causes hyperkalemia

Iatrogenic hyperkalemia occurs as a result of excessive parenteral potassium administration, especially in patients with chronic renal failure.

The release of potassium from cells is observed with hemolysis, tumor collapse syndrome, rhabdomyolysis, metabolic acidosis due to intracellular uptake of hydrogen ions (except in cases of accumulation of organic anions), insulin deficiency and plasma hyperosmolality (for example, with hyperglycemia), 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 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 attacks of muscle weakness or paralysis that occur in situations that promote the development of hyperkalemia (for example, during physical activity).

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

Hyperkalemia is often observed in oliguric acute renal failure due to increased cellular potassium release (due to acidosis and increased catabolism) and impaired potassium excretion.

Undiagnosed urinary tract obstruction is often the cause of hyperkalemia.

Impaired potassium excretion is also accompanied by drug nephritis, lupus nephritis, sickle cell anemia, and diabetic nephropathy.

Symptoms of Hyperkalemia

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 decreased cell excitability, muscle weakness occurs, including paresis and respiratory failure. In addition, ammoniogenesis, the reabsorption of ammonium ions in the thick segment of the ascending loop of Henle and, consequently, the excretion of hydrogen ions, is inhibited. The resulting metabolic acidosis aggravates hyperkalemia because it stimulates the release of potassium from the cells.

The most serious manifestations are due to the cardiotoxic effects of potassium. First, tall, 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 merging with the T wave leads to the formation of a curve resembling a sinusoid. Subsequently, ventricular fibrillation and asystole occur. In general, however, the severity of cardiotoxicity does not correspond to the degree of hyperkalemia.

Diagnosis of Hyperkalemia

Chronic hyperkalemia is almost always associated with impaired potassium excretion. If the cause of hyperkalemia is unclear and the patient does not have any manifestations of it, pseudohyperkalemia should first be suspected. Then exclude oliguric acute renal failure and severe chronic renal failure.

When collecting anamnesis, it is clarified whether the patient has taken medicines affecting potassium balance, and whether hyperkalemia is associated with excess potassium intake from food.

During a physical examination, attention is paid to signs of changes in the volume of extracellular fluid and BCC, and diuresis is determined.

The severity of hyperkalemia is assessed by a combination of clinical manifestations, ECG abnormalities and plasma potassium concentration.

With hyperkalemia, normally functioning kidneys excrete 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 transtubular gradient of potassium concentration below 10. This is usually observed with hypoaldosteronism or with a decrease in the sensitivity of the kidneys to mineralocorticoids. Tests with mineralocorticoids (for example, fludrocortisone) can clarify the cause.

For the differential diagnosis of primary adrenal insufficiency and hyporenin hypoaldosteronism, the level of renin and aldosterone in plasma is determined in the standing and lying position. Preparation for this study is carried out within 3 days. Its goal is to create moderate hypovolemia. To do this, limit sodium intake (no more than 10 mmol/day) and prescribe loop diuretics.

When the sensitivity of the kidneys to mineralocorticoids decreases, hyperkalemia occurs due to decreased sodium reabsorption or increased chlorine reabsorption. In the first case, a decrease in the volume of extracellular fluid and high level renin and aldosterone in plasma, in the second - vice versa.

Hypoaldosteronism leads to severe hyperkalemia only if combined with excess intake of potassium from food, renal failure, release of potassium from cells, or the use of drugs that impair potassium excretion.

Treatment of Hyperkalemia

Treatment depends on the degree of hyperkalemia and is determined by the plasma potassium concentration, the presence of muscle weakness, and ECG changes. Life-threatening hyperkalemia occurs when plasma potassium concentrations exceed 7.5 mmol/L. In this case, severe muscle weakness, disappearance of the P wave, expansion of the QRS complex, and ventricular arrhythmias are observed.

Insulin promotes the movement of potassium into cells and a temporary decrease in its concentration in plasma. 10-20 units of short-acting insulin and 25-50 g of glucose are administered (to prevent hypoglycemia; in case of hyperglycemia, glucose is not administered). The action lasts for several hours, 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 when only glucose is administered (due to the secretion of endogenous insulin).

Diuretics, cation exchange resins and hemodialysis are also used. With normal renal function, loop and thiazide diuretics, as well as their combination, increase potassium excretion. The cation exchange resin sodium polystyrene sulfonate exchanges potassium for sodium in the gastrointestinal tract: 1 g of the drug binds 1 mmol of potassium, resulting in the release of 2-3 mmol of sodium. The drug is prescribed orally in a dose of 20-50 g in 100 ml of 20% sorbitol solution (to prevent constipation). The effect occurs within 1-2 hours and lasts 4-6 hours. The concentration of potassium in plasma decreases by 0.5-1 mmol/l. Sodium polystyrene sulfonate can be administered as an enema (50 g of the drug, 50 ml of 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 necrosis.

Hemodialysis is the fastest and most effective way to reduce plasma potassium concentrations. It is indicated in cases of severe hyperkalemia when other conservative measures are ineffective, as well as in patients with acute renal failure and chronic renal failure. Peritoneal dialysis can be used to reduce plasma potassium concentrations, but it is significantly less effective than hemodialysis. Be sure to carry out treatment aimed at eliminating the cause of hyperkalemia. It includes diet, elimination of metabolic acidosis, increasing the volume of extracellular fluid, and the administration of mineralocorticoids.

Which doctors should you contact if you have hyperkalemia?

Anesthesiologist

Emergency doctor

Therapist

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

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

In case of kidney disease, and especially with low filtration capacity, a number of medications can cause hyperkalemia. These include:

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

Hyperkalemia can result from:

for autoimmune diseases, infections, transfusion of incompatible blood, poisoning with hemolytic poisons;
tissue breakdown due to malignant tumor;
damage to muscle fibers due to injury, dermatomyositis;
extensive burns;
increased blood acidity (acidosis);
insulin deficiency in diabetes mellitus;
the use of beta blockers, muscle relaxants, against the background of impaired metabolism or excretion of potassium;
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;
drug-induced and autoimmune nephritis;
urolithiasis, prostate hypertrophy, obstructing the outflow of urine.

A persistent 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 cells due to the active breakdown of proteins and acidification of the blood, and in case of chronic form pathology, hyperkalemia is explained by the weak filtration ability of nephrons.

Symptoms in adults and children

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

severe muscle weakness up to paralysis of the limbs (usually ascending, flaccid);
impaired speech clarity;
apathy, drowsiness;
dizziness;
shortness of breath, with an increase in ion concentrations, respiratory failure appears;
feeling of heart failure;
nausea;
increased sweating;
decreased urine output;
pain in the chest, stomach;
, turning into bradycardia or;
inhibition of intestinal motility.

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

A feature of the course of the pathology in young children is the appearance of the first signs when the potassium concentration exceeds 7 mmol/l. Frequent regurgitation, vomiting, adynamia, lethargy are noted, the heart rhythm, reflexes and intestinal motor function 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 conduction disturbances in the myocardium. The following typical signs appear on the ECG:

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

With the progression of electrolyte disturbances, sinusoidal waves are recorded instead of the typical P and QRS shape. If assistance is not provided at this stage, then complete blockade of impulse conduction or ventricular fibrillation develops, followed by asystole (cardiac arrest).

It should be noted that rhythm disturbances are not directly dependent on the potassium content 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.

ECG with increased potassium in the blood

Other diagnostic methods

First of all, when testing blood, it is necessary to exclude a false increase in potassium. It is associated with its release from cells when a sample is taken. This situation can occur with prolonged or intense pressure on the hand with a tourniquet, hemolysis, or a high concentration of leukocytes and platelets. When blood clots, potassium also moves into the extracellular space, which leads to an increase in its level.

In order to make a correct diagnosis, you need to:

measure concentrations in plasma rather than serum;
explore others;
take into account diuresis, renal filtration rate;
exclude the influence of medications and food;
conduct an analysis of 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 renal function does not require special treatment. If signs of arrhythmia appear, or the patient has renal failure, then therapy begins from the first minutes of diagnosis. The goal 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 up to 7 mmol/l, then the introduction of a cation exchange resin (sodium polystyrene sulfonate with sorbitol) is usually sufficient.

For higher values and changes in the electrocardiogram, calcium gluconate and sodium bicarbonate are administered. If this was not enough, then a drip with glucose and short-acting insulin is connected. All this time, monitoring of the electrolyte composition of the blood and ECG is necessary. In severe cases, hemodialysis is performed.

Drugs for adults

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

In case of aldosterone deficiency, it is necessary to provide its injection (Deoxycorticosterone acetate).

Diet for acute hyperkalemia

Potassium-rich foods are completely excluded from the diet. To do this, you need to follow these recommendations:

vegetables - all fresh are prohibited, only boiled, greens, avocado, lentils, beans, green peas, potatoes are not recommended;
fruits - there is a lot of potassium in bananas, melons, watermelon, citrus fruits, plums, apricots, grapes, cherries, pineapple, any dried fruits, so they are not allowed for patients;
You can’t eat meat, fish, you can eat no more than 100 g of boiled fish per day chicken liver or shrimp;
Rye and bran bread, buckwheat, soy, chocolate, cocoa, molasses, and nuts (especially peanuts) are removed from the menu.

Foods that are not allowed for hyperkalemia

Prevention measures

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

If long-term therapy with medications that affect potassium concentration is planned, then monitoring the filtration capacity of the kidneys and adjusting the dose when it decreases is mandatory. It is also important to monitor basic myocardial functions using an ECG.

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

For diagnosis, a blood test is performed and typical changes on the ECG are detected. A minor deviation can be adjusted with diet, and if clinical or ECG signs appear, urgent therapy is necessary. If medications are ineffective, hemodialysis is prescribed.