Confirmed hyperkalemia. In order to make a correct diagnosis, How to prevent hyperkalemia

In some cases, an increase in the amount of vitamins and minerals in the body causes severe malaise and even the development of various quite serious ailments. Such a violation of health can be provoked by many factors, they require close attention and adequate correction under the supervision of a doctor. A rather dangerous pathological condition of this kind is considered hyperkalemia. Let's talk on www.site how hyperkalemia is treated, what it is, what symptoms indicate it.

What is hyperkalemia?

The disease hyperkalemia is pathological condition, which is accompanied by an increase in the amount of potassium electrolytes in the blood, and at the same time poses a threat to human life. Patients with such an ailment require prompt and adequate medical care, as the disease can cause cardiac arrest due to untimely therapy.

It is known that the optimal level of potassium in the blood is 3.5-5 mmol/l. Approximately 98% of this substance is found in the cells, and the remaining two percent are present in the intracellular fluid (and in the blood as well).

Potassium is essential for achieving mass physiological processes, and an increase in its concentration in the blood can be provoked overconsumption or inefficient derivation of this element.

About how hyperkalemia manifests itself (symptoms of the disease)

Mild hyperkalemia can practically not make itself felt. Most often, it is diagnosed after a routine blood test or in the presence of changes in the electrocardiogram. In certain mild cases a form of hyperkalemia can be manifested by a violation of the rhythm of heart contractions, the patient feels them as a heartbeat.

More pronounced hyperkalemia usually causes more pronounced malaise. When conducting an ECG, high T-waves, increased ORS and P-R intervals become noticeable. In addition, the disease causes ventricular, severe muscle weakness. The doctor may note the appearance of cardiac arrhythmia, sharpening of the T wave on the electrocardiogram, as well as an increase in the amount of potassium up to 7 mmol / l or even more.

About how hyperkalemia is corrected (treatment of the disease)

Choice of therapy this violation depends solely on the causes of its development. In the event that the potassium level reaches 6.5 mmol / l or exceeds this figure, it is necessary to immediately take measures to reduce it to normal level. A similar effect can be achieved by introducing calcium (in the form of calcium chloride or). Such a drug is able to quickly and effectively neutralize the toxic effects of hyperkalemia. Excellent effect gives intravenous administration of a ten percent solution of calcium gluconate. Within one to five minutes, thirty to fifty milliliters of such a composition is injected.

It is worth noting that one ampoule of calcium chloride contains three times more calcium than calcium gluconate. Such a remedy begins to act within a few minutes (less than five), and the effect of its introduction lasts about half an hour to an hour. The dosage is selected against the background of constant ECG monitoring during administration.

In addition, to treat hyperkalemia and reduce the likelihood of complications, various medical manipulations that can temporarily stop the aggressive effects of potassium before it is removed from the body. Some patients are given ten to fifteen units of insulin intravenously (combined with fifty milliliters of fifty percent dextrose). Such therapy leads to a displacement of potassium ions into the cells and its effectiveness remains stable for several hours. In parallel, other corrective measures are being taken.

So, bicarbonate can also be used to shift potassium into the cells. Patients are given one ampoule over five minutes.

A good effect is also given by the use of salbutamol (albuterol or ventolin), beta 2-selective catecholamines in the amount of ten to twenty milligrams.

If hyperkalemia is particularly severe, the patient needs hemodialysis or hemofiltration. Such measures help to quickly and effectively eliminate excess potassium from the body. They are used when the underlying causes of hyperkalemia cannot be corrected quickly.

In order to reduce potassium levels over several hours, the patient is shown oral or rectal use of sodium polystyrene sulfate. Furosemide also helps to speed up the excretion of potassium along with urine.

How to treat hyperkalemia if it is not severe?

Patients with mild hyperkalemia should limit the amount of potassium in the diet to forty to sixty mmol / day. They should stop taking drugs that can slow down the excretion of potassium from the body. These drugs include potassium-sparing diuretics, NSAIDs, and ACE inhibitors.

To prevent severe hyperkalemia, it is also necessary to exclude the use of medications that can move potassium from the cells to the intracellular space. These drugs include primarily beta-blockers.

To accelerate the excretion of potassium from the body, loop and thiazide diuretics are used (in the absence of contraindications).

Hyperkalemia is a rather serious condition that requires immediate correction under the supervision of a doctor. Lack of adequate and timely therapy can pose a threat to the life and health of the patient.

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, in last years its prevalence is increasing. 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 the systemic level at the proper level. blood pressure and normal blood flow in vital important 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 a decongestant effect, activates many enzymes. In addition, it plays a key role in the processes of conducting 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, glands. internal secretion. Potassium prevents accumulation in the vessels and cells of the body excess sodium salts and thus 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 of it regulatory mechanisms functioned and interacted as harmoniously 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, by causing disturbances in cardiac contraction, it provokes a change in the course electrical processes in him. The consequence of this is: intoxication of the body, arrhythmia and even cardiac arrest. Therefore, even when mild form hyperkalemia treatment requires immediate, 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. Similar state provoke:

• 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 renal tissue, due to which hyperkalemia develops even with a reduced (in comparison with 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 epithelial tissue tubules to aldosterone, which is noted 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 types of cell damage and destruction that may occur due to destruction shaped elements blood (leukocytes, platelets, erythrocytes), with oxygen starvation, reducing the blood supply to tissues, as well as their necrosis; with the development of the syndrome prolonged crushing tissues, burns, cocaine overdose;
• 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, excess intake of potassium into the body with food or taken medicines does not cause persistent hyperkalemia.

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

Symptoms of hyperkalemia

Regardless of the causes of hyperkalemia, the disease on initial stages practically does not show up. On the this stage it is often diagnosed absolutely by accident during the delivery of tests or during the passage of an electrocardiogram. Before the only symptom hyperkalemia can be only a slight disturbance of the normal heart rhythm, which, as a rule, goes unnoticed by patients.

As you progress pathological process 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 (most early symptom 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 complex 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 formidable complication capable of progressing to death.

Timely identification of the causes of hyperkalemia and initial stages 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 treatment, for example, extracorporeal hemocorrection.

Normally, the concentration of extracellular potassium is in the range of 3.5-5.0 mmol/L. Laboratory indicators determinations of potassium in serum may vary slightly depending on 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.

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 emergency 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 kidney failure(determining the speed glomerular filtration, 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);
• impaired secretion of potassium distal parts nephron (congenital or acquired).

Renal failure with a significant decrease daily diuresis It is the most common cause 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 clinical condition, 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 delay urine, inadequate artificial ventilation lungs, hyperthermia, convulsions);
• termination of administration 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 the membranes of cardiomyocytes 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. Maximum effect insulin action 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 0.5 mg of salbutamol is able to lower the level of potassium in the 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 coronary disease cardiac administration of the drug through a nebulizer is preferred. 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 by using loop diuretics- in patients with preserved renal function to remove fluid. The use of furosemide (40-80 mg intravenously) in combination with isotonic saline sodium chloride blocks reverse suction 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 several hours after the introduction of the sorbent into 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. Increased sodium levels, tendency to constipation, decreased magnesium levels are the main side effects kayeksalata.

Performing hemodialysis. The inability to eliminate the cause of hyperkalemia, combined with the absence of positive effect from ongoing emergency treatment and the preservation of a life-threatening condition form indications for urgent execution procedures for renal replacement therapy.

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

Maximum quick removal potassium from the body is provided when 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 scheduled specifying diagnostic procedures and conservative treatment.

Treatment of non-life-threatening hyperkalemia

To not life threatening mild to moderate hyperkalemia refers to hyperkalemia with a plasma potassium level of up to 6.5 mmol / l inclusive and the absence of 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 of patients have a mild form of the disease (which is generally well tolerated). Any pathogen that provokes even a mild form of the disease must be quickly identified and eliminated in order to prevent progression to a more severe form. severe form. Severe hyperkalemia can lead to cardiac arrest and death.

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

Potassium promotes normal functioning nervous system and heart. It regulates the activity of smooth and skeletal muscles. Potassium is important for the transmission of electrical signals along nervous system. Optimal Levels potassium maintain normal heartbeat. 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 moderate hyperkalemia can cause changes in the ECG, and severe right rhythm heart rate, 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. Graduated from the Nizhny Novgorod medical academy(2007-2014) and residency in clinical laboratory diagnostics (2014-2016).

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