Also raise levels:

• Burns;
• Surgical intervention;
• Hemolysis (decay of red blood taurus),
• Mass lysis of tumor cells;
• Rabdomioliz.

High levels can be associated with certain health problems:

• Addison disease;
• Chronic kidney disease;
• Angiotensin glossy enzymes;
• Angiotensin II receptor blockers;
• Diabetes;
• Manifestations of oliguria;
• Difficult release of potassium kidneys with OPN and CPN.

Potassium is usually excreted by the kidneys, so violations that reduce the function of the latter can lead to hypercalemia. These include.

Description:

Hypercalemia is a condition in which the potassium concentration in the plasma exceeds 5 mmol / l. It arises as a result of potassium output from cells or disruption of potassium kidneys.

About potassium violations quickly signal ECG changes in Deletion II. In hypercalemia, pointed teeth are observed, and when they are flattened teeth and waves U.

Symptoms:

The resting potential is determined by the ratio of potassium concentrations inside the cell and in extracellular fluid. In hypercalemia, due to depolarization of cells and a decrease in cell excitability, muscle weakness occurs, right up to paresis and respiratory failure. In addition, ammoniogenesis is oppressed, ammonium ion reabsorption in the thick segment of the ascending part of the loop of Genla and, therefore, the elimination of hydrogen ions. The emerging exacerbates hyperkalemia, because it stimulates the output of potassium from cells.

The most serious manifestations are due to the cardiotoxic effect of potassium. First, high pointed teeth of T. In more severe cases, the PQ interval is extended and the QRS complex expands, the AV-Conduction is slowed down, the R. Teeth disappears, the expansion of the QRs complex and its fusion with the Tung Tung leads to the formation of a curve resembling a sinusoid. In the future, ventricular fibrillation occurs and. In general, however, the severity of cardiotoxic action does not correspond to the degree of hypercalemia.

Causes of occurrence:

Hypercalemia arises as a result of potassium output from cells or disruption of potassium kidneys. Increasing the consumption of potassium is rarely the only cause of hypercalemia, since thanks to adaptation mechanisms, its elimination rapidly increases.

Yatrogenic hypercalemia occurs as a result of excess parenteral administration of potassium, especially in patients with CPN.

Pseudogpercalemia is due to the yield of potassium from cells during blood takes. It is observed in violation of venopunction techniques (if the harness is tightened too long), hemolysis, leukocytosis, thrombocytosis. In the last two cases, potassium comes out of cells when the thrombus is formed. Pseudogperkalemia should be suspected if the patient has no clinical manifestations Hypercalemia and no reasons for its development. At the same time, in the correct blood and measurement of the concentration of potassium in plasma, and not in serum this concentration should be normal.

The output of potassium from cells is observed in hemolysis, tumor decay syndrome, rhabomiolesis, metabolic acidosis due to intracellular seizure of hydrogen ions (except for cases of accumulation of organic anions), insulin insufficiency and plasma hyperosmolyness (for example, when), treatment of beta-adrenoblockers (rarely occurs, but Hypercalemia due to other factors can be promoted, the use of depolarizing minelaxants, such as chloride succames (especially during injury, burns, neuromuscular diseases).

The physical activity causes transient hyperkalemia, following which hypokalemia may occur.

The rare cause of hypercalemia is a family hypercalemic periodic. This autosomal dominant disease is due to a single amino acid substitute in the protein of the sodium channel of transverse muscle fibers. The disease is characterized by attacks of muscle weakness or paralysis arising in situations that contribute to the development of hypercalemia (for example, during exercise).

Hypercalemia is also observed with severe due to the suppression of the activity of NA +, K + -at phase.

Chronic hypercalemia is almost always due to a decrease in the removal of potassium kidneys as a result of either violation of its secretion mechanisms, or reduce fluid flow in distal departments Nephron. The latter cause rarely independently leads to hypercalemia, however, it can contribute to its development in patients with protein deficiency (due to reduction of urea excretion) and hypovolemia (due to the reduced flow of sodium ions and chlorine to the distal nephron diversion).

Violation of the secretion of potassium ions arises as a result of a decrease in the reabsorption of sodium ions or an increase in the reabsorption of chlorine ions. Both then lead to a decrease in transverse potential in the cortical department of collecting tubes.

Trimethopris and Pentamidine also reduce potassium secretion by reducing sodium reabsorption in the distal nephron departments. Perhaps it is precisely the action of these drugs that hyperkalemia is explained, which often arises in the treatment of pneumatic in patients with AIDS.

Hypercalemia is often observed with oliguric OPN due to increasing potassium output from cells (due to acidosis and enhanced catabolism) and violations of its excretion.

When CPR, an increase in fluid flow into the distal nephron departments to a certain time compensates for a decrease in the number of nephrons. However, when the SCF becomes less than 10.15 ml / min, hypercalemia occurs.

Often the cause of hypercalemia is an undiagnosed obstruction of urinary tract.

Treatment:

For treatment prescribe:

Treatment depends on the degree of hypercalemia and is determined by the concentration of potassium in plasma, the presence of muscle weakness, changes to the ECG. Life-threatening hyperkalemia occurs with increasing potassium concentration in plasma more than 7.5 mmol / l. In this case, there is a pronounced muscular weakness, the disappearance of the teeth P, the expansion of the QRS complex, ventricular.

Urgent Care Shown in severe hypercalemia. Its goal is to recreate the normal rest potential, moving potassium into cells and enhancing the elimination of potassium. Caline the receipt of potassium from the outside, cancel drugs that violate its elimination. To reduce the excitability of myocardium, calcium gluconate, 10 ml of 10% solution in / in for 2-3 minutes is introduced. Its action begins a few minutes later and continues for 30.60 min. If after 5 minutes after the administration of calcium gluconate, the changes to the ECG are preserved, the drug is introduced re-in the same dose.

The movement of potassium into the cells and the temporary decrease in its plasma concentration promotes insulin. 10-20 units are injected short action and 25-50 g of glucose (for warning; when hyperglycemia, glucose is not administered). The action continues for several hours, already for 15-30 minutes, the concentration of potassium in the blood is reduced by 0.5-1.5 mmol / l.

Reducing the concentration of potassium, although not so fast, observed when administered only glucose (due to the secretion of endogenous insulin).

Sodium bicarbonate also contributes to the movement of potassium into the cells. It is prescribed with severe hypercalemia with metabolic acidosis. The drug should be administered as an isotonic solution (134 mmol / l). For this, 3 bicarbonate ampoules are diluted in 1000 ml of 5% glucose. When CPN, sodium bicarbonate is inffective and can lead to sodium overload and hypervolemia.

Beta2-adrenostimulants in parenteral or inhalation administration also contribute to the movement of potassium into the cells. The action begins after 30 minutes and lasts 2-4 hours. The plasma potassium concentration is reduced by 0.5-1.5 mmol / l.

Diuretics, cation exchange resins and hemodialysis are also used. With the normal function of kidney, loop and thiazide diuretics, as well as their combination increases the elimination of potassium. Cationi-exchange resin Polystyrenesulfonate sodium exchanges in the potassium trap on sodium: 1 g of the drug binds 1 mmol potassium, as a result, 2-3 mmol sodium is released. The drug is prescribed in a dose of 20-50 g in 100 ml of 20% sorbitol solution (for warning). The action occurs after 1-2 hours and lasts 4-6 hours. The plasma potassium concentration is reduced by 0.5-1 mmol / l. Sodium polystyreneculfonate can be administered as an enema (50 g of the preparation, 50 ml of 70% sorbitol solution, 150 ml of water).

Sorbitol is contraindicated in postoperative period, especially after kidney transplantation, as it raises the risk of colon.
- The fastest and efficient way to reduce potassium concentration in plasma. It is shown in the case of severe hypercalemia in the ineffectiveness of other conservative events, as well as patients with OPN and CPN. To reduce the concentration of potassium in plasma, it can be used, however, it is significantly inferior to hemodialysis. Be sure to conduct treatment aimed at eliminating the causes of hypercalemia. It includes a diet, elimination of metabolic acidosis, increasing the volume of extracellular fluid, the purpose of mineralocorticoids.

Hypercalemia Associated with a characteristic sequence of changes to the ECG. The earliest manifestation is a narrowing and sharpening in the form of a chaolash of the top of the T. T.
The Qt interval at this stage is shortened, corresponding to a decrease in the pliability of PD. Developing extracellular hypercalemia reduces the membrane potential of atrial and ventricular peace, thereby inactivating sodium channels that reduce Vmax and the speed of conducting. The QRS complex begins to expand, and the amplitude of the teeth p decreases. An extension of the PR interval may occur, which sometimes glorify AV-blocking II or III degree.

Full disappearance of teeth r It may be associated with a nodal replacement rhythm or with the so-called synovantricular conduct (with synovativericular conductivity there is no causability of the myocardium atrial at the intact conductive system.

At the same time, the impulse from the sinus unit is carried out on the ventricles through the AV-connection to form a pseudo-cheerful - without teeth of the EGG - rhythm with narrow ventricular complexes.
This is a "hidden sinus rhythm", which is rapidly loaded).

At a later period The development of hypercalemia The sinus pulse is carried out from the CA node to the Av-node, but the clear teeth P is not formed.
Moderate and severe hypercalemia is sometimes manifested in the form of Elevation of ST in the right-wing infants (V1 and V2) and simulates ischemic damage current or configuration observed during Brugada syndrome. However, even severe hypercalemia may have atypical or undiagnosed changes to the ECG.

Very pronounced hypercalemia in the presence of some additional conditions leads to asistolia, sometimes with the preceding slow wave-like (sinusoidal) vulgarization of the ventricles.

Triadconsisting of high, with pointed vertices of teeth (as a result of hypercalemia) elongated (as a result of hypocalcemia) and GLB (as a result arterial hypertension), is a highly sensitive sign of chronic renal failure.

As a result of electrophysiological changesassociated with hypokalemia, on the contrary, the CMC membrane membranes occurs and the duration of PD increases. The main ECG sign of this deviation from the norm is ST Depression with compressed teeth and increased teeth U. U. Teeth can exceed the amplitude of the T. T.

Clinically separation of teeth T And the teeth u on surface ECG may be difficult or even impossible. Visible teeth U for hypokalemia and other pathological conditions can be, indeed, part of the teeth of T, the shape of which changes under the influence of the voltage gradient between M-cells, or mid-sicardial cells, and adjacent myocardial layers.

The lengthening of repolarization during hypokalemia as part of the acquired elongated Qt (U) syndrome predisposes to the emergence of Torsades de Pointes tachycardia. Hypokalemia when taking digitalis also increases the likelihood of tachyarhythmia.

Training video decoding ECG in electrolyte violations

Hyperkalemia is called a condition in which the level of serum potassium exceeds 5 mmol / l. Hypercalemia occurs in 1-10% of patients hospitalized in hospitals.

Hyperkalemia is called a condition in which the level of serum potassium exceeds 5 mmol / l. Hypercalemia occurs in 1-10% of patients hospitalized in hospitals. The number of patients with hyperkalemia has increased in recent years due to an increase in the number of patients receiving medicines affecting the renin angiotensin-aldosterone system (RAAS).

Potassium is the most important electrolyte of the human body. He plays a key role in conducting nerve impulses and cut muscles. 98% of potassium focused on intracellular fluid, potassium concentration here reaches 140 mmol / l. Outside the cells there is only 2% potassium, the concentration here is 3.8-5.0 mmol / l.

The role of potassium in the body

Potassium - The main intracellular cation (positively charged ion), in contrast to sodium - the main extracellular cation.

Functionally potassium and sodium are interconnected:

• Creating a membrane potential important to muscle contraction (skeletal and heart muscle) is ensured by maintaining high concentration Sodium outside the cell and potassium inside the cell (sodium-potassium pump, see cris 1).
• Maintaining acid-base equilibrium, osmotic balance, water balance
• Activation of many enzymes

Mechanisms for regulation of potassium exchange

To maintain a normal potassium balance (transport between intra and extracellular fluid) requires a well-coordinated interaction of all regulatory mechanisms. The main mechanism of regulation of potassium level is highlighting it kidneys. This mechanism is controlled by the adrenal hormone aldosterone. The presence of this mechanism ensures that, despite the high potassium content in food (from 40 mmol to 200 mmol), its blood serum will be maintained at a constant level. Violation of the regulation of potassium level, and, as a result, increasing it in the blood can change the excitability of membranes. So, the function of nerves, muscles, hearts will be disturbed.

Aldosterone - Mineralcortic hormone, synthesized in cholesterol adrenal cortex. Under the action of aldosterone in the kidneys, the canalzia reabsorption increases (that is, the reverse absorption from the primary urine) sodium ions: aldosterone stimulates sodium transitions inside the cells, and potassium is outward (in the intercellular space, that is, potassium goes into the urine, released from the limit) - cm .ris.2. Aldosterone also increases the secretion of potassium and hydrogen kidney. Thus, the organism increases the content of sodium and extracellular fluid (water is held in the body). The level of aldosterone depends on the level of sodium (Na +) and potassium (K +). With a high concentration of potassium and low sodium concentration, the synthesis and the secretion of the aldosterone is amplified. The most important impact on the level of aldosterone is a renin-angiotensin system (see Paras). Other factors also affect the level of aldosterone.

Many factors participate in the development of hyperkalemia, which develops as a result of reducing potassium allocation or increasing potassium output from cells.

Hypercalemia can be false (pseudo-boiler), it must be excluded primarily (except in cases where emergency assistance is required).

Pseudo-boiler

Table 1: Causes of pseudo-boiler

• Not in time performed analysis
• Blood fence from veins in which potassium was introduced
• Too strong pressure when applying a harness or intensive work with a fist for fist
• Hemolysis when blood flow through a thin needle or traumatic venopunction
• Long storage of blood
• High leukocytosis or thrombocytosis (significantly elevated level leukocytes or platelets)
• Unusual genetic disorders (family hypercalemia)

Hypercalemia with increased flow of potassium

Excessive flow of potassium with food can contribute to hypercalemia if parallel decreases the release of potassium with urine. With the normal kidney function, all potassium should be output.

Table 2: High potassium products

• Salt substitutes
• Syrup
• Bran, cereals, wheat sprouts
• Vegetables (spinach, tomatoes, carrots, potatoes, broccoli, Limskaya beans, cauliflower) and mushrooms
• Dried fruits, nuts, seeds
• Fruits (bananas, kiwi, oranges, mango, melon)

Hypercalemia may be associated with hemotransphus - intravenous administration Blood cells from which potassium comes into extracellular space, with too fast administration of calcium preparations for the treatment of hypokalemia, with high potassium content during parenteral nutrition.

Hypercalemia associated with the yield of potassium from cells

Some exogenous and endogenous factors may disrupt potassium exchange between the intercellular and intracellular fluids and increase serum potassium concentration. However, this mechanism rarely causes severe hyperkalemia, except in cases where the factor is, for example, tissue damage, necrosis (local fabric death as a result of damage), rhabomiolysis, tumor disintegration, severe burns.

Table 3: Reasons for the redistribution of potassium Redistribution of potassium between extracellular and intracellular liquids

• Muscle necrosis, MIIZ (Rabbomioliz - Skeletal Muscle Damage), Tumor Disintegration, Heavy Burns
• Insulin deficiency (Normally, this hormone speeds up moving potassium into cells)
• Metabolic acidosis
• Hyperosmolarity (hyperglycemia - improving blood glucose levels, administration of mannitol)
• Medicines (for example, succinylcholine (it is dichilin, leafenon), beta blockers, digoxin)
• Hypercalemic periodic paralysis (attacks develop most often 30-40 minutes after exercise)

• Kidney damage (glomerular filtration<20 мл/мин)
• Reducing the activity of mineralkorticoids
• Hypheninemiasis of hypoaldosteroneism (chronic diseases of the kidneys, diabetic nephropathy, NSAIDs)
• Advanced deficiency (Addison's disease, congenital enzyme defect)
• Aldosterone blockers (see Table 4)
• Unresponsibility to aldosterone (sickle-shaped anemia, systemic red lupus, amyloidosis, obstructive nephropathy)

• Hypovolemia
• Some genetic disorders, such as Gordon Syndrome (Gordon's Syndrome)

Hypercalemia caused by a disturbance of potassium allocation

The main part of potassium is excreted by the kidneys, so the kidney damage is the main cause of hypercalemia. The defeat of the kidneys accounts for up to 75% of cases of this state.

In patients with chronic kidney diseases, potassium is maintained until renal failure is developing (when filtration is reduced less than 15-20 ml / ml) or in cases where the patient consumes a large number of potassium or takes drugs that increase potassium levels .

Damage to the YUCSTAGLOMAERAL ACTION leads to a deficiency of Renin production (seeRas), which causes hyponatremia and hypoaldosteronism, which can also cause hyperkalemia even in the absence of severe kidney damage. Himbroneinemic hypoaldosteroneism is also known as 4 type type 4 type channel, as it is often associated with a light or moderate severity with metabolic acidosis, with a normal anionic gap (the difference between cations and anions; ANION GAP \u003d (Na + K) - (CL +) (units Measurements - mol / l)). Most often this state is developing in diabetic nephropathy.

Also, hypoaldosteronism may be a consequence of primary adrenal disease (Addison disease, congenital violations of steroid synthesis, 21-hydroxylase deficiency) or a decrease in mineral corticito-shaped activity. The latter problem is often associated with sickle-shaped anemia, a systemic red lupus, amyloidosis, obstructive nephropathy, using potassium-saving diuretics. In rare cases, the mutation of the mineralcorticoid receptor gene is revealed.

In general, violation of mineralcorticoid exchanges does not cause hyperkalemia if the normal amount of sodium falls into the distal nephron. Thus, not always in patients with Addison disease, hypercalemia develops if they have adequate salt consumption. Violation of the urinary or delivery of sodium to the distal nephron plays an important role in the development of hypercalemia. These disorders can be caused by internal factors or (more often) by some drugs (see Paintts 3, 4).

Medications causing hypercalemia

Medicinal preparations may violate potassium homeostasis in several mechanisms: activation of potassium transmembrane transport, decrease in renal excretion (change in aldosterone, sodium delivery to distal nephron, changing the function of collecting tubes). Risk increases when such drugs take patients with renal failure. Elderly patients and patients with diabetes are especially susceptible to the development of hypercalemia. In these groups, such drugs should be used with caution, starting with small doses and controlling the level of potassium every time the dose change. There is no recommendation for the number of studies, the rate of determination of potassium level depends on the level of renal failure, the presence of diabetes, taken drugs concomitant.

In particular, it is very carefully necessary to follow patients with impaired electrical conductivity of the heart muscle, since even a minor increase in potassium content can lead to arrhythmias.

Full list of drugs - in the table.

Medicines that violate transmembrane transport of potassium

• Beta blockers
• Digoxin
• Hyperosmolar solutions (mannitol, glucose)
• Suksmetonius (leafenon)
• Intravenous introduction of positively charged amino acids

• Kaliva additives
• Salt Substitutes.
• Vegetable preparations (alfalfa, dandelion, horsetail, sofa, nettle)
• Red blood cells (with their destruction, potassium is released)

Medicines that reduce the secretion of aldosterone

• APF inhibitors
• Angeiotensin II receptor blockers
• NSAID (NSAID)
• Heparin preparations
• Antifungal preparations (ketoconazole, fluconazole, intractrazol)
• Cyclosporins
• Program

Medicinal substances that block the binding of aldosterone and mineral corticidal receptors

• Spironolakton
• Inspra (EPLERENONUM)
• Chrospirenone

Preparations inhibiting the activity of potassium channels in epithelial cells

• Potassybean diuretics (amyloride, triamtenen)
• Trimethopris (antimicrobial drug)
• Pentamidine (antimicrobial drug)

Let us dwell on some of them:

Inhibitors of angiotensin-converting enzyme (Angiotensin Converting Enzyme (ACE) inhibitors) and angiotensin II receptor blockers (Angiotensin II RECEPTOR BLOCKERS (ARBS)) are actively used to protect the kidneys and reduce mortality from heart disease, especially in diabetics. They are also included in standard diagrams of treating patients with chronic heart disease.

These drugs predispose to the development of hypercalemia, since the secretion of aldosterone is disturbed and reduced reperfusion in the kidneys (and the level of glomerular filtration). Both drugs reduce the release of potassium with urine.

They do not cause hypercalemia in patients with normal kidney function; The degree of aldosterone is not sufficient for a significant violation of potassium excretion, if there was no preceding hypoaldosteroneism (due to some disease or reception of other drugs). Unfortunately, people taking these drugs have a high risk of hypercalemia. About 10% of outpatient patients hypercalemia develops over a year after the start of treatment with AFP inhibitors or angiotensin II receptor blockers.

Moreover, these drugs contribute to the development of hyperkalemia in 10-38% of patients delivered to hospitals. At the same time, the risk is especially elevated if the patient takes high or doses of drugs or in combination with other drugs causing hyperkalemia.

Aldosterone receptor antagonists are also often used in the treatment of CONGESTIVE CARDIAC FAILURE patients since The Randomized Aldactone Evaluation Study has shown that the addition of spironolactone in the treatment decreases the number of complications and mortality. In this study, it is indicated that heavy hypercalemia developed only in 2% of patients, when the level of creatinine concentration was 106 mmol / l, and the dose of spiroranolactone did not exceed 25 mg per day. In contrast, Population Based Time-Series Analyses, demonstrate a significant increase in hospitalization and mortality from hypercalemia. This is probably because the study includes patients with severe renal function, taking high doses of spironolactone. These patients more often than others in the study take potassium additives or other preparations that violate potassium allocation. The risk increases with a combination of spiroranolactone with AFP and ARBS inhibitors, especially in elderly patients with impaired kidney function.

Non-steroidal anti-inflammatory drugs (NSAIDs, non-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS)) inhibit renin secretion (which leads to hypoaldosteroneism and reduce the excretion of potassium kidneys) and can break the kidney function. These drugs can set Judiciously in patients with diabetes or renal failure, especially if patients take other drugs (ACE and ARBS inhibitors).

Hypercalemia often proceeds without symptoms and is detected with a laboratory study. When symptoms are, they are not specific, and mainly associated with impaired muscle functions (paresthesia, muscle weakness, fatigue) or heart functions (palpitations).

ECG: high "peak" teeth t, alignment or absence of teeth P, extension of the QRS complex, Sine Waves.

Nevertheless, the ECG is not a sensitive method of diagnosing hypercalemia. In the study of Acer and colleagues, almost half of patients with potassium level above 6.5 mmol / l were no changes to the ECG. In addition, some patients have a gradual change in the function of the heart, and others have quick progress from benign changes to fatal ventricular arrhythmias.

Examination of patients with hyperkalemia should include:

• Careful analysis of the history of the disease to identify potential risk factors, such as impaired kidney function, diabetes, adrenal insufficiency, the use of drugs that can cause hyperkalemia.
• Laboratory tests should be aimed at confirming the history of the disease and physical examination, and should include urea, creatinine, electrolytes, osmolarity (acute increase in osmolarity can cause potassium output from cells), as well as the analysis of potassium concentration in the urine.
• In some patients, additional special tests are carried out, such as the definition of sodium fractional excretion or a transceiver potassium gradient can be used to distinguish between the renal and waste causes of hypercalemia.

What to do with severe hyperkalemia?

Hypercalemia management guidelines are based on expert opinions, since there is a lack of clinical studies. Treatment should be directed to the restoration of electrolyte metabolism, the prevention of serious complications and the treatment of the underlying disease. Light or moderate hypercalemia drawing is used loop diuretics to increase the excretion of potassium. Potassium consumption with food must be limited. Dose of drugs that increase blood potassium level should be reduced as much as possible or cancel. If the patient has a violation of the kidney function, diuretics may be ineffective. Then other measures are required, in particular, conducting dialysis.

Heavy hypercalemia is a life-threatening state, as it can cause serious impairment of the heart and a neuromuscular system that includes stopping the heart and palsy muscles. Consequently, urgent and aggressive therapy is required. Many authors lead the following criteria for severe hypercalemia: more than 6.0 mmol / l + changes to the ECG or more than 6.5 mmol / l regardless of the presence of changes to the ECG.

If there are signs of hyperkalemia on ECG or in the case of a heart stop in patients on dialysis, for example, therapy begins without laboratory data. Other factors that require proactive treatment: rapid rise in potassium level, characteristic of acidosis, rapid deterioration of the kidney function.

Most recommendations and experts are advised in severe hypercalemia treatment should be carried out under a hospital, which allows for continuously monitoring cardiac activity, as even in patients without symptoms and changes to the ECG may develop arrhythmia threatening life.

Although emergency dialysis removes potassium from the body, it is necessary to urgently begin treatment of the underlying disease, since Cochrane Systematic Review of Emergency Interventions for Hyperkalamia recommends simultaneously three things:

• First step is the stabilization of myocardial activities, reduced the likelihood of arrhythmia. Intravenous calcium is used as a direct potassium antagonist when influencing membrane, stabilizing cardiac conductivity. Calcium gluconate in a volume of 10 ml of 10% solution is introduced within 3-5 minutes under the control of the heart on the cardiomonitor. Calcium infusion does not affect the level of serum potassium, but has an impact on the work of the heart: the changes to the ECG are visible in 1-3 minutes after calcium administration, the Last for 30-60 minutes effect. Infusion can be repeated if the effect does not occur within 5-10 minutes. It should be very careful to apply calcium in patients receiving digoxin, since calcium enhances the toxic effects of digoxin.
• Second Step- Translation of potassium from extracellular fluid into intracellular. This reduces the level of serum potassium. It is achieved by the introduction of insulin or beta-2-agonists, which stimulate the sodium-potassium pump. Insulin is introduced intravenously in a sufficient amount of glucose (to prevent hypoglycemia). The effect of insulin administration occurs after 20 minutes, reaches a maximum after 30-60 minutes, is preserved up to 6 hours. From selective beta-2-agonists, salbutamol is most often used. Salbutamol is used using nebulizer The effect occurs after 20 minutes, the maximum action is 90-120 minutes. Salbutamol can be used one or in a combination with insulin. Patients with acidosis can also be appointed sodium bacarbonate, although the question of the benefits of this drug during hyperkalemia still remains controversial.
• Thirdly, measures are being held to eliminate potassium from the body. The potent loop diuretics (for example, 40-80 mg of furosemide intravenously) increase the renal excretion of potassium by increasing the urica and sodium delivery to the distal nephron. But diuretics only work with the saved kidney function, and many patients with hyperkalemia have sharp or chronic renal diseases. Cation-exchange resins that remove potassium from extracellular fluid in exchange for sodium through the intestines are also used widely, although their effectiveness is controversial. They act faster in the form of the enema than with oral administration. The achievement of the effect may take 6 hours. Dialysis is final for the treatment of patients with severe hyperkalemia and progressive kidney disease.

After emergency assistance, measures must be taken to prevent the repetition of hypercalemia. First of all, it should be analyzed by the patient medication. If possible, reduce or cancel drugs that increase the level of potassium. Since AFP inhibitors and angiotensin II receptor blockers slow down the progression of chronic renal diseases, the use of other measures to control hyperkalemia or a reduction in the dose of the drug is more preferable than the cessation of these preparations. It is reasonable to limit potassium consumption to 40-60 mmol per day. Also, the use of diuretics can also be effectively. Thiazide diuretics can be used in patients with saved kidney function, but they are usually ineffective if the glomeric filtering is less than 40 ml / min, when looper diuretics are more preferred. Fludrocortisone can be used in patients with hypheninemiasis hypoaldosteronism. However, this drug should be used with caution, especially in patients with type 2 diabetes, which often proceeds with hypertension, as the drug leads to a fluid delay and pressure increase.

• In patients without predisposition to hyperkalemia, repeat the analysis of potassium to eliminate pseudo-boilers.
• Do not forget about possible hidden causes of hypercalemia, including NSAIDs
• ACE inhibitors and angiotensin II receptor blockers must be appointed with small doses, the potassium level should be monitored one week after the start of treatment and after a dose increases
• All patients with hyperkalemia must pass ECG (12 assignments)
• Changes to ECG and arrhythmia associated with hyperkalemia, require urgent medical care.

• How important is the contribution of various risk factors in the development of hypercalemia and how to evaluate them?
• With the increase to use cardio- and renoprotectors that contribute to the holding of potassium, which method is most preferable to control the level of potassium?

A deeper understanding of molecular mechanisms underlying maintaining the level of potassium in extracellular fluid, the development of new therapeutic strategies for the treatment of hypercalemia threatening life.

Hypercalemia is an increased maintenance of potassium in the blood exceeding the concentration of 5.5-6 mmol \\ l. Violation of the electrolyte balance may cause excessive consumption of potassium, potassium excretion disorders or transmembrane movement of ions.

The cause of hypercalemia is often polyethological, most often due to renal failure, the actions of medicines and hyperglycemia. Since healthy faces can adapt to excessive potassium intake, increasing its elimination, the increased power of potassium in the diet is rarely the only etiological factor in hyperkalemia, often the primary impairment of the kidney function often.

Violation of the excretion of potassium

Hypercalemia due to the pathology of the kidneys arises due to such pathophysiological mechanisms: a violation of the speed of blood flow in distal nephrons, the secretion of aldosterone and its actions, the functioning of potassium secretion paths in the kidneys. Hypercalemia caused by a violation of the distal transportation of sodium and water occurs when stagnant heart failure, acute damage to the kidneys and the terminal stages of chronic kidney disease. Pathology, which can cause hypoaldosteronism (frequent complication of diabetic nephropathy and tubula interstacious diseases), can lead to hypercalemia.

Transmembrane moving electrolyte

Different mechanisms contribute to the movement of potassium from cells or into cells, thus increases the concentration of potassium in the blood plasma (redistribution hypercalemia). Due to the increased osmolarity of blood plasma, for example, with an uncontrolled flow of diabetes mellitus, a concentration gradient arises when potassium ished along with water from the cells. The relative deficiency of insulin or resistance to it also often happens in diabetics, which prevents the movement of potassium into the cells. In response to acidosis, extracellular hydrogen ions exchange for intracellular potassium, even though the final result is very variable and partially dependent on the type of acidosis. The greatest effect is observed in metabolic acidosis. Since 98% of all potassium potassium contains intracellularly, any process that is accompanied by increased destruction of cells, such as rhabdomiolysis, tumor lysis syndrome or hemotransphusion, can lead to hypercalemia.

Hypercalemia due to the action of medicines

Medicines often cause hyperkalemia, especially in people with renal failure or hypoaldosteronism. Most often, hypercalemia happens when the drugs violate the elimination of potassium. Also, the additional purpose of potassium for correction or hypokalemia prevention may accidentally lead to hypercalemia.

According to one study, approximately half of the cases caused by hypercalemia with drugs was due to the ACE inhibitors, and approximately 10% of outpatient patients who began treatment with an ACE inhibitor or angiotensin receptors, hypercalemia arose during one year. The frequency of hypercalemia associated with potassium-saving diuretics has significantly increased, since it has been proven that in patients with stagnant heart failure, the addition of spironolactone to standard therapy reduces the incidence and mortality. With the simultaneous assignment of an APE inhibitor and an angiotensin receptor inhibitor there is a risk of dangerous side effects, including hypercalemia, so the combination is avoiding a combination. Other popular drugs that can cause hyperkalemia include trimethopris, heparin, B-blockers, digoxin and NSAIDs.

Diagnosis and treatment of hypercalemia

As with hypocalemia, the danger of hypercalemia is the negative impact on the heart conductivity and the reduction of muscles, so the initial measures are aimed at the diagnosis of whether a Urgent intervention is needed. The absence of symptoms does not allow to eliminate severe hypercalemia, since this pathology often flows asymptomatic. Given the increased risk of developing hypercalemia, patients with renal failure need special attention.

Diagnostics

Anamnesis and physical examination.

Heavy hypercalemia may cause muscle weak, ascending paralysis, tachycardia and paresthesia. The risk of developing hypercalemia increases such pathology as chronic kidney diseases, diabetes mellitus, heart failure and liver disease. Find out which drugs takes the patient, as some of them can cause hyperkalemia; Also asked if the sick substitutes containing potassium. During physical examination, pay attention to the blood pressure and state of the BCC in order to eliminate the potential reasons for the reduction of kidney perfusion as the etiology of hypercalemia. Neurological symptoms of hypercalemia include generalized weakness and reduction of tendon reflexes.

Laboratory examination and ECG

Re-determining the level of potassium in serum helps to diagnose pseudo-boilers, which often happens due to the movement of potassium from cells during or after sampling. Other laboratory tests are also shown: the level of creatinine and urea in the serum, the level of creatinine and electrolytes in the urine, the assessment of acid-alkaline equilibrium. Further examination may include the determination of the level of glucose in serum to eliminate hyperglycemia, determining the level of renin, aldosterone and cortisol to assess the function of the kidneys and adrenal glands.

If the potassium level exceeds 6 mmol / l, there is symptoms of hypercalemia, suspicion of the rapid development of hypercalemia, if in patients with primary diseases of the kidney, heart or cirrhosis there was a new case of hypercalemia - an ECG is performed. The changes to the ECG are not specific or sensitive to the diagnosis of hypercalemia. Therefore, although the changes to the ECG are an indication for urgent medical measures, the decision on therapeutic tactics is not based exclusively on the presence or absence of changes to the ECG.

The pointed teeth are the most early ECG signs of hyperkalemia. Other changes to the ECG include a flat tooth of P, the elongation of the PR interval, the expansion of the QRS complex. Hypercalemia can lead to arrhythmias: sinus bradycardia, sinus blockade, ventricular tachycardia, ventricular fibrillation and asistolia.

Treatment

The goal of urgent events is the prevention of potentially dangerous violations of cardiac conductivity and neuronal disorders, intracellular movement of potassium, elimination of excessive potassium from the body and the corresponding geometasis disorders. Patients with chronic hyperkalemia are advised to reduce potassium intake with food. Although the redistribution hypercalemia happens infrequently, during treatment, it is necessary to be careful and not attempt to increase the elimination of potassium, since the correction of primary pathology can provoke the development of hypokalemia - "ricochet". Indications for emergency intervention: symptoms of hypercalemia, changes to ECG, severe hypercalemia, rapid development of hypercalemia or the presence of heart disease, cirrhosis or kidney disease. It is important to control the potassium level often, since patients belong to the risk risk group of hyperkalemia, until the course of the primary disease is adjusted and excess potassium from the body is removed.

Emergency care for hypercalemia

The introduction of calcium, which stabilizes the cardiomyocyte membranes and thus contributes to the prevention of the development of hazardous conductivity disorders, is shown in the presence of appropriate changes to the ECG. The introduction of calcium does not affect the concentration of potassium in the blood plasma. If after 5 minutes after the introduction on the control ECG, the signs of hypercalemia are visible, the calcium dose is repeated. Duration of calcium administration Short: from 30 to 60 min.

Insulin and glucose. The most reliable method of moving potassium ions intracellular is the introduction of insulin with glucose. Usually introduced 10 units. Insulin, after which 25 g of glucose is also introduced for the prevention of hypoglycemia. Since hypoglycemia is a frequent side effect even with the introduction of glucose, regularly monitor the level of glucose in serum.

Inhalation β2 agonists. Albuterol - selective β2-adrenomimetic - It is a popular preparation to move potassium intracellularly. The drug is effective for any method of administration: inhalation, intravenous or with a nebulizer. It should be noted that the recommended dose of albuterol when administered with a nebulizer is 10-20 mg 4-8 times higher than the usual respiratory dose. When combination with insulin, an additive effect is observed. Albuterola's ability to reduce potassium level in some patients is broken, especially with the terminal stage of kidney disease, so this drug cannot be used as monotherapy.

Bicarbonate of soda. Although it is often used to treat hypercalemia to treat, these evidence-based medicine are ambiguous, demonstrate minimal benefits or in general the absence of any effect. Therefore, sodium bicarbonate is not used in monotherapy mode. Soda can play a role as adjuvant therapy, especially in patients with concomitant metabolic acidosis.

Reducing the total content of potassium in the body.

Potassium can be removed from the body through the gastrointestinal tract, kidney or directly from the blood using dialysis. Dialysis is shown to patients with renal failure or threatening hyperkalemia or with the ineffectiveness of other measures. Other treatments do not act fairly quickly for the urgent correction of hypercalemia.

Ion-exchange resins available in the market (usually polystyrene sodium polystyrene (KayExalate / Caxhalate) are not provided for the treatment of the acute phase of hypercalemia, but can be effective to reduce the total potassium content in the body in a subacute period. Since Polystyrene Sodium can cause constipation, many pharmacological funds with a laxative purpose. Contain sorbitol. However, there are reports of clinical cases of damage to the gastrointestinal tract with a combined application of a sodium polystyrene-sulfonate with sorbitol, so the FDA (USA) agency officially warned about danger. Recent information about side effects related to the monotherapy of the sodium polystyrentsulfonate. Therefore, this drug is in combination with sorbitol or in mode Monotherapy Avoid in patients from a risk group or with an existing intestinal function, such as postoperative patients or patients with constipation or inflammatory bowel disease.

There is no evidence of the effectiveness of diuretics in the acute phase of hypercalemia. However, diuretics, especially loop, can play a certain role in the treatment of certain types of chronic hypercalemia, especially due to hypoaldosteronism. Fludrocortisone - a drug of choice in hypercalemia associated with a deficiency of mineralocorticosteroids, including hypoaldosteronism.

Measures for the prevention of chronic hypercalemia include a diet, poor potassium, cancellation or correction of the dose of certain preparations, the departure from the NSAID, the use of diuretics with the saved kidney function.