Disorders of the water and electrolyte balance. Violation of the water and electrolyte balance Water electrolyte body balance

Electrolyte balance and its violations in the human body

The electrolyte balance in the human body is equilibrium anions (potassium, sodium, etc.) and cations (organic acids, chlorine, etc.).

Disturbance of the exchange of potassium

The role of potassium in the organism is multifaceted. It is part of proteins, which causes an increased need for it when anabolic processes are activated. Potassium is involved in carbohydrate exchange - in the synthesis of glycogen; In particular, glucose passes inside the cells only with Cali. It also participates in the synthesis of acetylcholine, as well as in the process of depolarization and repolarization of muscle cells.

Disturbance of potassium exchange in the form of hypokalemia or hypercalemia accompany the diseases of the gastrointestinal tract quite often.

Hypokalemia may be a consequence of diseases accompanied by vomiting or diarrhea, as well as in disabilities of suction processes in the intestine. It may occur under the influence of long-term use of glucose, diuretics, heart glycosides, adrenolytic drugs and in insulin treating. Insufficient or incorrect preoperative preparation or postoperative maintenance of the patient - poor potassium diet, infusion of potassium solutions, can also lead to a decrease in potassium content in the body.

Potassium deficiency can manifest a feeling of tingling and gravity in the limbs; Patients feel severity in centuries, muscle weakness and fast fatigue. They are sluggish, they have a passive position in bed, slow intermittent speech; Disturbance can appear, transient paralysis and even disorders of consciousness - from drowsiness and spin to coma development. Changes from the cardiovascular system are characterized by tachycardia, arterial hypotension, an increase in the size of the heart, the appearance of systolic noise and signs of heart failure, as well as a typical picture of the ECG changes.

Hypokalemia simpotomas

Hypokalemia is accompanied by an increase in sensitivity to the action of muscle relaxants and the elongation of their action, slowing the awakening of the patient after surgery, atonium of the gastrointestinal tract. Under these conditions, hypokalemic (extracellular) metabolic alkalosis can be observed.

Correction of hypokalemia

Correction of the lack of potassium should be based on the exact calculation of its deficiency and is carried out under the control of the content of potassium and the dynamics of clinical manifestations.

During the correction of hypokalemia, it is necessary to take into account the daily need in it, equal to 50-75 mmol (2-3 g). It should be remembered that in different salts of potassium contains its different amount. Thus, 1 g of potassium is contained in 2 g of potassium chloride, 3.3 potassium citrate and 6 g of potassium gluconate.

Hypokalemia treatment

Potassium preparations are recommended to be administered as a 0.5% solution with glucose and insulin at a rate not exceeding 25 mmol per hour (1 g of potassium or 2 g potassium chloride). At the same time, careful control of the condition of the patient, the dynamics of laboratory indicators, as well as the ECG in order to avoid overdose.

At the same time, there are research and clinical observations showing that with pronounced hypokalemia, parenteral therapy is properly selected in terms of volume and set of drugs may and should include significantly more potassium preparations. In some cases, the amount of potassium intimidated 10 times exceeded the recommended dose; At the same time there was no hypercalemia. However, we believe that the overdose of potassium and the danger of unwanted effects is real. Caution with the introduction of large quaria potassium is needed, especially if it is not possible to ensure permanent laboratory and electrocardiographic control.

Hypercalemia reasons

Hypercalemia may be a consequence of renal failure (the removal of potassium ions from the body), massive transfusion of canned donor blood, in particular the long-term storage time, insufficiency of adrenal function, increased decay of tissues during injury; It may occur in the postoperative period, with an excessively rapid introduction of potassium preparations, as well as with acidosis and intravascular hemolysis.

Symptoms

Clinically hypercalemia is manifested by the feeling of "crawling of goosebumps", especially in the limbs. At the same time, impairment of muscles, a decrease or disappearance of tendon reflexes, disorders of the heart in the form of bradycardia. Typical ECG changes are to increase and pointed the teeth, lengthening the P-Q interval, the appearance of ventricular arrhythmia, up to the heart fibrillation.

Hypercalemia treatment

Hypercalemia therapy depends on its severity and causes. With pronounced hypercalemia, accompanied by severe heart activities, the re-intravenous administration of calcium chloride is shown - 10-40 ml of 10% solution. During moderate hypercalemia, you can use intravenous administration of glucose with insulin (10-12 UR insulin per 1 l 5% solution or 500 ml of 10% glucose solution). Glucose contributes to the movement of potassium from extracellular space into intracellular. With concomitant renal failure, peritoneal dialysis and hemodialysis is shown.

Finally, it should be borne in mind that the correction of the concomitant disorders of the acid-base state - alkalosis for hypokalemia and acidosis in hyperkalemia - also contributes to the elimination of potassium balance disorders.

Sodium exchange

Normal sodium concentration in blood plasma is 125-145 mmol / l, and in red blood cells - 17-20 mmol / l.

The physiological role of sodium is its responsibility for maintaining the osmotic pressure of extracellular fluid and the redistribution of water between the extracellular and intracellular medium.

Sodium deficiency can develop as a result of its losses through the gastrointestinal tract - with vomiting, diarrhea, intestinal fistulas, with loss of kidney during spontaneous polyuria or forced diuresis, as well as with abundant sweating through the skin. Less often, this phenomenon may be a consequence of glucocorticoid deficiency or excessive generation of antidiuretic hormone.

Hyponatremia Causes

Hyponatremia may occur in the absence of external losses - with the development of hypoxia, acidosis and other reasons causing an increase in the permeability of cell membranes. In this case, the extracellular sodium moves inside the cells, which is accompanied by hyponatremia.

Sodium deficiency causes a redistribution of fluid in the body: the osmotic pressure of blood plasma is reduced and intracellular hyperhydration occurs.

Symptoms of sodium deficiency

Clinically hyponatremia manifests quickly fatigue, dizziness, nausea, vomiting, decrease in blood pressure, convulsions, violations of consciousness. As can be seen, these manifestations are nonspecific, and to clarify the nature of the violations of the electrolyte balance and the degree of their severity, it is necessary to determine the sodium content in blood plasma and red blood cells. This is necessary for directed quantitative correction.

Hyponatremia Treatment

With a true sodium deficiency, the sodium solutions of chloride should be used, taking into account the magnitude of the deficit. In the absence of sodium losses, measures are needed to eliminate the reasons for increasing the permeability of membranes, the correction of acidosis, the use of glucocorticoid hormones, proteolytic enzyme inhibitors, mixtures of glucose, potassium and novocaine. This mixture improves microcirculation, contributes to the normalization of the permeability of cell membranes, prevents the reinforced transition of sodium ions inside the cells and thereby normalizes the sodium balance.

Hypernatremia Causes

Hypernatremia arises against the background of oliguria, limitations of injected fluids, with overpressing sodium, in the treatment of glucocorticoid hormones and ACTH, as well as in primary hyperaldosteroneism and Cushing syndrome. It is accompanied by an impaired water balance - extracellular hypershydration, manifested by thirst, hyperthermia, arterial hypertension, tachycardia. Evenkers can develop, increase intracranial pressure, heart failure.

Hypernatremia Treatment

Hypernatremia is eliminated by the appointment of aldosterone inhibitors (Veroshpiron), limiting sodium administration and normalization of water exchange.

Calcium exchange

In the normal functioning of the body of calcium plays an important role. It increases the tone of the sympathetic nervous system, congestives tissue membranes, reduces their permeability, increases blood clotting. Calcium has a desensitizing and anti-inflammatory effect, activates the macrophage system and the phagocytic activity of leukocytes. The normal content of calcium in the blood plasma is 2.25-2.75 mmol / l.

Hypocalcemia reasons

In many diseases of the gastrointestinal tract, disorders of calcium metabolism develop, resulting in an excess, or a deficiency of calcium containing blood plasma. Thus, with acute cholecystitis, acute pancreatitis, saworoduodenal stenosis, hypocalcemia occurs due to vomiting, calcium fixation in the foci of steatonecosis, increase the content of glucagon. Hypocalcemia may occur after massive hemotransphusion therapy due to calcium binding with citrate; In this case, it can also be relative in nature due to the flow of significant quasi in the body contained in canned blood. The decrease in calcium content may be observed in the postoperative period due to the development of functional hypocorticism, which causes calcium care from blood plasma into the bone depot.

Hypocalcemia symptoms

Hypocalcemia treatment

Therapy of hypocalcemic conditions and their prevention consist in intravenous administration of calcium-chloride or gluconate drugs. The prophylactic dose of calcium chloride is 5-10 ml of a 10% solution, therapeutic - may increase to 40 ml. It is preferable to carry out therapy with weak solutions - not higher than 1 percent concentration. Otherwise, the sharp increase in the calcium content in the blood plasma causes the chims of calcitonin by the thyroid gland, which stimulates its transition to the bone depot; In this case, the concentration of calcium in the blood plasma may fall below the original.

Hypercalcemia reasons

Hypercalcemia for diseases of the gastrointestinal tract is much less common, but it may occur under peptic ulcer, stomach cancer and other diseases, accompanied by the depletion of the function of the adrenal cortex. Hypercalcemia is manifested by muscle weakness, total patient intensity; Possible nausea, vomiting. With the penetration of significant amounts of calcium inside the cells, lesions of the brain, heart, kidneys, pancreas can develop.

Magnesium exchange in human body

The physiological role of magnesium is to activate the functions of a number of enzyme systems - the atphase, alkaline phosphatase, cholinesterase, etc. It is involved in the implementation of the transmission of nerve impulses, ATP synthesis, amino acids. The concentration of magnesium in the blood plasma is 0.75-1 mmol / l, and in red blood cells - 24-28 mmol / l. Magnesium is quite consistently persisted in the body, and it is infrequently developing losses.

Gipicomagnation - Causes and Treatment

Nevertheless, the hypomagnemia occurs during long-term parenteral nutrition and pathological losses through the intestines, as magnesium is absorbed in the small intestine. Therefore, magnesium deficiency can develop after an extensive resection of the small intestine, with diarrhea, sublicasy fistulas, during the intestinal paresis. The same violation may occur against the background of hypercalcemia and hypernatremia, in the treatment of cardiac glycosides, with diabetic ketoacidosis. Magnesium deficiency is manifested by an increase in reflex activity, cramps or muscle weakness, arterial hypotension, tachycardia. Correction is carried out by solutions containing magnesium sulfate (up to 30 mmol / day).

Hypermagnias - causes and correction

Hypermagnias occurs less frequently of the hypomagnia. The main causes are renal failure and massive tissue destruction leading to the release of intracellular magnesium. HyperMagnias can develop against the background of insufficiency of adrenal function. It is manifested by a decrease in reflexes, hypotension, muscle weakness, violations of consciousness, up to the development of deep coma. HyperMagnias is corrected by eliminating its causes, as well as peritoneal dialysis or hemodialysis.

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Intracellular water (70%) is associated with potassium and phosphate, main cation and anion. Extracellular water is about 30% of its total amount in the body. The main cation of the extracellular fluid is sodium, and the anions are bicarbonates and chlorides. The distribution of sodium, potassium and water is presented in Table. five.

Table 5. Distribution of water, sodium and potassium in the body of a man weighing 70 kg (total water - 42 liters (60%) weight) (according to A. U. Wilkinson, 1974)
Indicator	Extracellular liquid			Fluid intracellular
	Plasma	Interstitial	Transolellar	Soft fabrics	Bone
Total water,%	7	17	6	60	10
Volume, L.	3	7	2	26	4
Sodium	44% of the total, 39.6 g, or 1723 MEKV			9% of the total, 8.1 g, or 352 MEKV	47% of the total, 42.3 g, or 1840 MEKV
Potassium	2% of the total, 2.6 g, or 67 MEKV			98% of total, 127.4 g, or 3312 MEKV

According to A. U. Wilkinson (1974), the plasma volume is 1/3 of the interstitial fluid. Every day, 1100 liters of water, 8 liters of fluid secrets 1100 liters between blood and intercellular fluid, is secreted in the intestinal lumen and reabsorb.

• Sodium exchange violations

  Sodium blood contains 143 MEKV / L, in the intercellular space 147, in 35 MEKV / l cells. Sodium balance disorders can manifest itself in the form of a decrease (hypontremia), an excess of it (hypernatremia) or changes in the distribution in various environments of the body with a normal or modified total amount of it in the body.

  Reducing the amount of sodium can be true or relative. True hyponatremia is associated with loss of sodium and water. This is observed in case of insufficient intake of salt, abundant sweating, with extensive burns, polyuria (for example, in chronic renal failure), intestinal obstruction and other processes. Relative hypontremia occurs when an aqueous solution of aqueous solutions with a speed exceeding the selection of water by the kidneys.

  According to A. W. Wilkinson (1974), clinical manifestations of sodium deficiency are determined primarily by speed, and then its loss value. Slow loss of 250 MEEs sodium causes only a decrease in performance and appetite. Fast loss of 250-500 and especially 1500 MEKV sodium (vomiting, diarrhea, gastrointestinal fistula) leads to severe blood circulation disorders. Sodium deficiency, and with it and water reduces the volume of extracellular fluid.

  The true excess of sodium is observed in the introduction of salt solutions, increased consumption of salt, delayed sodium dedication by the kidneys, excessive products or long-term administration from the outside of gluco- and mineralcorticoids.

  The relative increase in sodium in the blood plasma is observed during dehydration.

  True hypernatremia leads to hyperhydration and the development of edema.

• Disturbance of the exchange of potassium

  98% of potassium is in intracellular and only 2% in extracellular fluid. In the blood plasma of human, the norm is due to 3.8-5.1 MEKV / l potassium.

  The daily balance of potassium in humans was compiled by A. U. Wilkinson (1974). Changes in potassium concentration below 3.5 and above 7 MEKV / l are considered pathological and designated as hypo and hypercalemia.

  Important in the regulation of the number of potassium in the body belongs to the kidney. Control of this process is carried out by aldosterone and partially glucocorticoids. There is an inverse dependence between the pH of the blood and the content of potassium in plasma, i.e., with acidosis, potassium ions extend from cells in exchange for hydrogen and sodium ions. Reverse changes are observed during alkalosis. It has been established that when the cell of three potassium ions is out ofward, two sodium ions and one hydrogen ion comes. With a loss of 25% of potassium and water, the cell function is broken. It is known that with any extreme impacts, for example, during starvation, potassium leaves cells into an interstitial space. In addition, a large number of potassium is released by proteins catabolism. Therefore, due to the effects of aldosterone and cortisol, the renal mechanism is included, and potassium is intensively secreted into the lumen of the distal tubules and is highlighted in large quantities with urine.

  Hypokalemia is observed in excessive products or the introduction of the outstanding aldosterone, glucocorticoids that cause excessive secretion of potassium in the kidneys. Reducing potassium is also noted with intravenous administration of solutions, insufficient flow of potassium into the body with food. Since potassium excretion occurs constantly, hypokalemia is formed under these conditions. Potassium loss also occurs with the secrets of the gastrointestinal tract during vomiting or diarrhea.

  With potassium deficiency, the function of the nervous system is disturbed, which manifests itself in drowsiness, rapid fatigue, slow-minded vague speech. The excitability of the muscles is reduced, the motility of the gastrointestinal tract deteriorates, the systemic blood pressure decreases, the pulse is replenished. The ECG is detected to slow down the conductivity, a decrease in the flip of all teeth, an increase in the Qt interval, the shift of ST segment below the isoelectric line. An important compensatory reaction aimed at maintaining the constancy of potassium in blood plasma and cells is the limitation of its excretion with urine.

  The main causes of propelleamia are the disintegration of the protein during starvation, injury, decrease in the volume of circulating blood (dehydration and especially the violation of the secretion K + in the conditions of oligo- and anuria (acute renal failure)), excessive administration of potassium in the form of solutions.

  Hypercalemia is characterized by muscle weakness, hypotension, bradycardia, which can lead to a heart stop. On the ECG, a high and acute teeth of T, the broadening of the QRS complex, the flattening and disappearance of the Zub R.

• Magnesium exchange violations

  Magnesium performs an important role in activating many enzyme processes, in carrying out the excitation of nervous fibers, in muscle contraction. According to A. W. Wilkinson (1974), in an adult, a weight of 70 kg contains about 2000 MEKV magnesium, while Potassium 3400 MEQ, and sodium 3900 MEQ. About 50% of magnesium is in the bones, as much - in the cells of other tissues. In extracellular fluid it is less than 1%.

  In adults in the blood plasma contain 1.7-2.8 mg% magnesium. The main mass of it (about 60%) is in ionized form.

  Magnesium, like potassium, is an essential intracellular element. In the exchange of magnesium, kidneys and intestines take part. Absorption is carried out in the intestines, and its secretion is constant in the kidneys. Between the exchange of magnesium, potassium and calcium there is a very close connection.

  It is believed that the bone tissue serves as a source of magnesium, easily mobilized in the event of a deficiency in the cells of soft tissues, and the mobilization process of magnesium from the bones is faster than the replenishment of it from the outside. With magnesium deficiency, calcium balance is violated.

  Magnesium deficiency is observed during starvation and reduction of its absorption, with a loss with secrets of the gastrointestinal tract as a result of fistula, diarrmy, resectations, as well as its secretion enhanced after introducing sodium lactate into the body.

  The definition of symptoms of magnesium deficiency is very difficult, but it is known that the combination of magnesium deficiency, potassium and calcium is characterized by weakness and apathy.

  An increase in magnesium in the body is observed as a result of a violation of its secretion in the kidneys and enhancing the decay of cells in chronic renal failure, diabetes, hypothyroidism. An increase in magnesium concentration over 3-8 MEKV / L is accompanied by hypotension, drowsiness, inhibition of breathing, the absence of tendon reflexes.

• Violation of water balance

  The water balance in the body depends on the receipt and removal of water from the body. Water loss, especially in pathology, can fluctuate. Water exchange disorders are closely interconnected with electrolyte balance and manifest themselves in dehydration (dehydration) and hydration (increasing the amount of water in the body), the extreme expression of which is swelling.

Edema (ODEMA) It is characterized by excessive accumulation of fluid in the tissues of the body and serous cavities. It is thus accompanied by hyperfatering of intercellular spaces with simultaneous impaired electrolyte balance in cells and their hyper-or hyphydration (BME, vol. 18, p. 150). Water delay is due to the accumulation in the sodium body of the main osmotic cation.

The main general mechanisms for the formation of edema

Under the edema, a huge amount of fluid can accumulate as a result of violations of water-electrolyte metabolism in tissues. In this process, a number of mechanisms take part.

Dehydration - This is a pathological process characterized by a disadvantage of water in the body. Two types of dehydration (Kerpel - Fronius) are distinguished:

1. Water loss without an equivalent amount of cations. This is accompanied by the thirst and the redistribution of water from the cells in an interstitial space.
2. Sodium loss. Compensation of water and sodium compensation comes from extracellular fluid. Characteristic is a violation of blood circulation without the development of thirst.

With dehydration caused by full starvation, people decrease the mass of the body, the diuresis is reduced to 600 ml / day, the proportion of urine is increased to 1.036. The sodium concentration and the volume of erythrocytes do not change. At the same time, dry mouth mucosa arises, thirst, and residual nitrogen is growing in the blood (A. W. Wilkinson, 1974).

A.U. Wilkinson proposes to classify dehydration on aquatic and salt. True "water exhaustion, primary, or simple, dehydration" caused by a lack of water and potassium, as a result of which the volume of intracellular fluid changes; Characterized by the thirst and Oligira. In this case, the osmotic pressure of the interstitial fluid is initially increasing, and therefore water moves from cells into extracellular space. In connection with the developing oliginia, the amount of sodium is maintained at a stable level, and potassium continues to be secreted in the distal tubules and stand out with urine.

True "salt exhaustion", secondary, or extracellular, dehydration is mainly connected with a lack of sodium and water. In this case, the volume of plasma and interstitial fluid decreases and the hematocrit is increasing. Therefore, it is the main manifestation of blood circulation.

The most serious losses of sodium are found in surgical practice and are due to the release of the gastrointestinal secretion through extensive wound surfaces. In tab. 6 The amount of electrolytes in plasma and various secrets of the digestive tract is presented.

The main causes of salt dehydration are sodium loss with a secreter exhausted (for example, in the operated patients), vomiting, gastrointestinal fistula, intestinal obstruction. Sodium loss can lead to a critical reduction in the volume of extracellular liquid and plasma and circulatory impairment, accompanied by a hypotension and a decrease in glomerular filtration.

With dehydration caused by both a deficiency of water and sodium loss, the normalization of the water and electrolyte balance is achieved by simultaneously administering sodium and water.

A source: Ovsyannikov V.G. Pathological physiology, typical pathological processes. Tutorial. Ed. Rostov University, 1987. - 192 p.

Surgical patients with the basic principles of violation of the water and electrolyte balance are outdoor or internal waters and electrolyte. Domestic losses are due not only to the pathological distribution of fluid between the water sectors, but also the phenomenon of sequestration in the "third" space (paretically bloated stomach, a thin or colon, abdominal cavity). Since in clinical practice, the diagnosis is amenable to disruption of water and electrolyte metabolism in an extracellular space or in a vascular bed, depending on the excess or lack of water distinguish between two types of dishydriy - extracellular hyperhymitation and extracellular dehydration.

Classification, pathogenesis:

Before proceeding with the consideration of various types of dishydrium, it is necessary to dwell on the modern ideas and principles of physiological regulation, as well as on some of the most important and accessible to the study of physico-chemical indicators of the internal media fluids and their clinical significance.

Volmia - blood volume in the body. This is a non-permanent value. It depends on:

Blood deposit;

Blood exposure;

Transcapillary exchange.

The body volume of the body is divided between two sectors: functioning (heart, veins, arteries, venela, arterioles and 10% of the capillary channel) and non-functioning (90% of the capillary bed). The capacity of the body's circulating blood is 7% of the body weight. 20% of this volume is in parenchymal organs, the remaining 80% of the circulating blood is in the cardiovascular system. In the depot of the body is the amount of blood equal in its volume - the volume of circulating blood.

Water in the body is located and distributed over three basins and is 60% of the body weight. Of them:

15% emerkane liquid;

5% volume of circulating blood;

40% tissue fluid.

Given the fact that at the present stage, the electrolytic composition of only the vascular bed is practically amenable. Only indirectly, focusing on the electrolyte and protein composition of the vascular bed can be judged on the quantitative and qualitative composition of the intercounted and tissue fluid. Consequently, in the future we will focus on the quantitative and qualitative composition of electrolytes, proteins in vascular bed.

Water in the body is only in the associated state. Free water for cells is poison. It binds to colloidal structures, in particular with proteins, fats and carbohydrates. These forms of water existence in the body are in constant motion and mutual equilibrium. Moving between the pools occurs under the influence of three forces: mechanical, chemical and osmotic. The so-called moving equilibrium is controlled by three stabilizing states: isotonia, isohydra and isoione.

All sectors and swimming pools containing water are closely related to each other, there are no isolated losses in the body!

Violation of the water balance in the body is called dyshydria. Dzhidria is divided into two large groups: dehydration and hyperhydration. Depending on the predominance of disorders in the extracellular or intracellular space, extracellular and intracellular forms of violations are distinguished. At the concentration of plasma electrolytes, hypertensive, isotonic and hypotonic dyshydrias are distinguished. The so-called associated dyshydriums are a combination of dehydration of one of the aquatic spaces with the hypershydration of the other.

Dehydration. Depending on the severity of dehydration, three degrees of dehydration are isolated: light, middle and heavy.

Degredation degrees:

Easy degree is characterized by a loss of up to 5-6% of the entire body fluid.

The average degree corresponds to a deficiency of 5-10% liquid (2-4 l).

A severe dehydration degree - fluid loss exceeds 10% of all water water resources (over 4-5 liters).

Acute loss of 20% of the fluid is deadly.

Associate violations. These violations arise in connection with the change in osmolarity and the movement of the fluid from one sector to another. As a result, dehydration can be observed in one sector, for example, at the same time in the other - hyperhydration. An example of such a form can be a hyperosmolar coma.

Hypershydration. In practice, the treatment of patients in intensive care departments and intensive care is hyperhydrated - the same frequent phenomenon as dehydration. An example is the associated forms of disorders, states accompanied by water delay in the body, sharp heart and renal failure, secondary aldosteroneism, etc.

Clinical symptoms:

To identify the disorders of the balance of water and electrolytes is not always easy. The diagnosis is established on the basis of the following clinical symptoms and laboratory data:

Thirst (availability, degree, duration);

Skin condition, language, mucous membranes (dry or humidity, elasticity, skin temperature);

Swelling (severity, prevalence, hidden swelling, change in body weight);

General symptoms (lethargy, apathy, adamina weakness);

Neurological and mental status (inadequacy, disorders of tendral reflexes, violation of consciousness, manic state, coma);

Body temperature (increasing due to thermoregulation disorders);

Central (blood pressure, heart rate, central venous pressure) and peripheral (nail bed blood flow, other signs) blood circulation;

Breathing (respiratory frequency, ventilation reserves, hypo- and hyperventilation);

Diuresis (amount of urine, its density, signs of renal failure);

Plasma electrolytes, hematocrit, acid-alkaline state, residual nitrogen, osmolarity, concentration of general protein, number of erythrocytes.

Separate forms of disorders of water salt equilibrium:

It is advisable to allocate six forms of dyshydrium, which actually unite all forms of violations of water balance and osmolarity:

Dehydration is hypertonic, isotonic, hypotonic;

Hypershydration is hypertonic, isotonic, hypotonic.

Hypertensive dehydration. It occurs if water loss exceeds the loss of electrolytes. The hypertensive dehydration leads an alimentary restriction of water intake and insufficient replenishment of its losses in comatose and other states, when the regulation of water exchange is broken, or water intake is not possible through the mouth. This form of dehydration occurs with significant losses of fluid through the skin and respiratory tract - with a fever, abundant sweating or artificial ventilation of the lungs, which is carried out without sufficient humidification of the respiratory mixture. Water deficiency may occur as a result of the use of concentrated electrolyte solutions and parenteral nutrition.

In the clinical picture, symptoms of water deficiency prevail (thirst, reaching an extreme degree of severity), dry skin, language and mucous membranes, increasing body temperature. As a result of an increase in plasma osmolarity, water deficiency is developing in cells, which is manifested by excitation, anxiety, delicious state and a coma. Opesolarness of urine increases.

Isotonic dehydration. Observed with fluid losses, the electrolyte composition of which is close to the composition of the plasma and interstitial fluid. The most common cause of isotonic dehydration is the loss of liquid during vomiting, diarrhea, acute and chronic diseases of the gastrointestinal tract, from gastric and intestinal fistulas. Isotonic losses arise with multiple mechanical injury, burns, appointing diuretics, isostenuria. Pronounced dehydration is accompanied by the loss of all major electrolytes. The osmolarity of plasma and urine does not significantly change.

General symptoms with isotonic dehydration are manifested faster than with hypertensive dehydration.

Hypotonic dehydration. It occurs with the true deficiency of sodium and to a lesser extent of water with fluid losses containing a large amount of electrolytes (for example, from the gastrointestinal tract), salts loss (polyuria, osmotic diuresis, Addison disease, strong sweating), reimbursement of isotonic losses with solutions that do not contain electrolytes. As a result, the decrease in plasma osmolarity and the entire extracellular fluid from the water deficit suffer mainly cells.

The most important clinical symptoms: a decrease in the turgore of the skin and tissues, soft eyeballs, circulatory disorders, reducing plasma osmolarity, oliguria and azotemia. Rapid decrease in plasma osmolarity (hemodialysis, peritoneal dialysis) can lead to a brain echo, cramps and coma.

Hypertensive hypershydration. It is observed with the introduction of large amounts of hypertensive and isotonic solutions of electrolytes (sodium chloride, bicarbonate, etc.), especially patients with renal failure, as well as conditions leading to an increase in antidiuretic hormone and aldosterone products (stress, adrenal diseases, acute glomerulonephritis, cardiovascular - seeming insufficiency).

With this form of violation, general symptoms are dominated: thirst, redness of the skin, an increase in blood pressure and central venous pressure, an increase in body temperature, neurological and mental disorders, in severe cases - delirium and coma. Characteristic sign - body swelling. From the very beginning of the disease, renal failure can manifest. The greatest danger represents the sharp heart failure, which can develop suddenly, without prudent symptoms.

Isotonic hyperhydration. It occurs when the lusters of large quantities of isotonic solutions containing sodium and diseases, accompanied by edema (cardiovascular failure, toxicosis of pregnancy, Cushing's disease, secondary aldosteroneism, etc.). In this case, the total content of sodium and water in the body is increased, but the concentration of NA + in plasma and the interstitial fluid remains normal.

Despite the hyperfedration, the body's need for free water is not fully satisfied and thirst arises. The flooding of the body isotonic fluid can lead to a number of complications: acute cardiovascular failure; acute renal failure, especially in patients with kidney disease; It is difficult to predictable disorders of the sectoral distribution between the vascular and interstitial sectors, which largely depends on the colloid-osmotic plasma pressure.

Hypotonic hyperhyrastration. Hypotonic hyperhyrastration is observed when the introduction of very large quantities of belligent solutions, with eats associated with the insufficiency of blood circulation, liver cirrhosis, acute renal failure and hyperproduction of antidiuretic hormone. This form of disorders may be observed with long-term exhausting diseases leading to a decrease in body weight.

Clinical symptoms of organism poisoning with water are developed: vomiting, frequent watery chair, polyuria with low urine density, then Anuria. As a result of flooding cells, symptoms associated with the lesion of the central nervous system are early appear: apathy, lethargy, violation of consciousness, convulsions and coma. In the late stage there are edema of the body. The blood circulation is not significantly violated, since the volume of fluid in the vascular sector does not significantly increase. The concentration of sodium and other electrolytes in the plasma is reduced.

Disorders of water and electrolyte exchange at CMT are multidirectional changes. They arise due to the reasons that can be divided into three groups:

1. Industrials typical for any resuscitation situation (identical at CMT, peritonitis, pancreatitis, sepsis, gastrointestinal bleeding).
2. Activities specific to brain lesions.
3. Thenogenic disorders caused by the forced or erroneous use of pharmacological and non-farmacological treatments.

It is difficult to find another pathological condition in which such a variety of water and electrolyte disorders would be observed, both at the THMT, and was so much a threat to life with their untimely diagnosis and correction. To understand the pathogenesis of these disorders, we will stop more in the mechanisms regulating water-electrolyte exchange.

A little physiology
Three "Whale", which keeps the regulation of water and electrolyte exchange is an antidiuretic hormone (ADG), a renin-angiotensin-aldosterone system (RAAS) and a atrial sodium system (PFF) (Fig. 3.1).

ADG affects reabsorption (that is, on the reverse absorption) of water in the renal tubules. When switching on the starting mechanisms (hypovolemia, arterial hypotension and hyposmolability) from the rear lobe of the pituitary gland is thrown into the blood of ADG, which leads to water delay and vasoconstrictions. The secretion of ADG stimulates nausea and angiotensin II, and slows down - the PFF. With excessive production ADG, the syndrome of excessive production of antidiuretic hormone (SIVADG) is developing. To implement the effects of ADG, in addition to the adequate functioning of the rear lobe of the pituitary gland, the normal sensitivity of specific adg receptors in the kidneys is needed. When decreasing the production of ADG in the pituitary gland, the so-called central unacceptable diabetes develops, when the sensitivity of the receptors is violated - nephlogenic non-ferrous diabetes.

Raas affects sodium kidney. When the starting mechanism (hypovolemia is turned on), there is a decrease in blood flow in YuCstamedullar glomes, which leads to the emission of Renin's blood. The increase in the level of renin causes the conversion of inactive angiotensin I to active angiotensin II. Angiotensin II induces vasoconstriction and stimulates the emission of minocuticoid-aldosterone with adrenal glands. Aldosterone causes water and sodium delay, in exchange for sodium ensures the removal of potassium and calcium due to the reversible blockade of their channel reabsorption.
The PNF can be considered as a hormone antagonist for ADG and RAAS. With an increase in the volume of circulating blood (hypervolemia), the pressure in the atrialists increases, which leads to the emission of the PNF in the blood and contributes to the removal of sodium by the kidneys. According to modern data, the TSFF acts in the same way, a low molecular weight compound, sampled in the hypothalamus. Most likely, an excess of Wabaina is responsible for the development of cerebral solventing syndrome.

3.1.1. Mechanisms of violation of the regulation of water and electrolyte exchange at CMT
Durademic violations are observed at any resuscitation situation. CMT is no exception to this rule. Activation of all units of regulation of water and electrolyte exchange during brain damage occurs due to the development of hypovolemia. At CMT, the mechanisms of the regulation disorder mechanisms are also included. They are launched in damage to the diancephal colors of the brain and violation of the hypothalamus bonds with a hypophysia due to direct injury, the increase in brain dislocation or vascular disorders. The result of the activity of these specific mechanisms is characteristic of cerebral pathology to change the production of ADG, Wabaine, trop hormones of the front lobe of the pituitary gland (for example, adrenocorticotropic hormone, indirectly affecting the level of aldosterone).

Hypertensive solutions, optimized hyperventilation, hypothermia used to relieve intracranial hypertension are forced nutritional measures, deepening water-electrolyte disorders. The use of saluretics at CMT most often (but not always!) Is an example of using drugs on erroneous indications, which causes rough impaired water and electrolyte balance.

Dysfunction of hormones regulating the water-electrolytic balance leads to violations of the voltage status (hypo- and hypervolemia), sodium content (hypo- and hypernatremia), osmolality (hypo and hyperosmolyality). Disorders of potassium content, magnesium, calcium, acid-base state are noted. All these disorders are interrelated. However, we will begin with a description of sodium concentration disorders, which is a central ion that regulates the osmotic blood pressure and determining the balance of water between the intravascular channel and the interstitial space of the brain.

Sodium disorders

Hypernamentia
Hyper Natremia, depending on the presence of volting disorders, is divided into hypovolemic, elamic and hypervolemic. Hypernatremia is always accompanied by an increase in efficient blood osmolality, that is, is hypertonic.

Hypovolemic hypernatremia
Hypovolemic hypernatremia is most often noted at the initial stages of the CMT. The causes of hypovolemic hypernatremia at this stage - renal and extreme losses of fluid, not compensated by sufficient flow into the body. It often occurs blood loss, as well as combined damage. Since the victim is in a changed consciousness, it loses the opportunity to adequately react to water losses through the kidneys and the skin. A frequent symptom of intracranial hypertension is vomiting. Therefore, fluid losses through the gastrointestinal tract can also play a significant role in the development of hypovolemia. It is also possible to move the fluid into the so-called third space due to sequestration in the paretic intestine.

The result of the activation of the described mechanisms is hypovolemia. The body is trying to compensate for the loss of intravascular volume by attracting fluid from the interstitial space. This prostation is dehydrated, but the attached fluid is not enough for "filling" of intravascular space. As a result, extracellular dehydration occurs. Since water is mainly lost, the sodium level in the extracellular sector (interstitial and intravascular space) increases.

Hypovolemia launches another hypernatremia mechanism: hyperaldosteroneism develops, which leads to a delay in sodium body (J.j. Marini, A.P. Wheeler, 1997). This reaction is also adaptive, since the osmotically active properties of sodium allow water to delay in the body of water and compensate for hypovolemia. At the same time, sodium delay leads to compensatory removal of potassium, which is accompanied by a number of negative consequences.

The inclusion of the described pathological mechanism is possible in later periods of CHMT, however, such pronounced hypovolemia, as in the early stages, is not noted, since the patient is already treated for this moment.

Eupolemic hypernatremia
This type of hypernatremia occurs when the loss of water loss over the loss of sodium is predominant. It is observed with the deficiency or inefficiency of ADG, using diuretics, syndrome reinstallation of osmostat.
The ADG deficiency is called tasteless, inset diabetes, Diabetes Insipidus (as the urine contains few salts) and otherwise the central unacceptable diabetes. The central unacceptable diabetes occurs due to direct damage to the pituitary gland or the violation of its blood supply. The syndrome is characterized by a violation of the production of ADG and is accompanied by hypernatremia due to excessive release of hypotonic urine with low sodium content. The treatment of syndrome is reduced to the use of synthetic substitutes of antidiuretic hormone and the correction of water losses.

The ineffectiveness of ADG, otherwise called nephrogenic nonaxar diabetes, can develop with concomitant diseases of the kidneys, hypercalcemia, hypokalemia. Chronic reception of some drugs (for example, lithium during depressive disorders) can reduce the sensitivity of renal receptors to the action of ADG.

Loop diuretics, such as furosemide, have an unpredictable effect on the removal of sodium and water. In some situations, more water may be raised than sodium, resulting in hypernatremia. It is assumed that the mechanism of this phenomenon is associated with the influence of the loop diuretic on the sensitivity of the renal adg receptors, that is, actually represents a variant of nephrodic non-ferrous diabetes. In other cases, more sodium is lost than water, and hyponatremia develops.

Osmostat reinstallation syndrome is a peculiar state, which is characterized by the establishment of a new normal blood sodium level and the corresponding change in its osmolality. According to our data, at QMS, the syndrome of reinstallation of ossemostat more often leads to the appearance of a lower, and not higher sodium norm, so we will consider it in more detail in the section dedicated to hyponatremia.

Hypervolemic hypernatremia
This form of hypernatrotemia is rare at the THMT. It always arises soerly. The main reason is the introduction of an excess of sodium-containing solutions - hypertensive (3-10%) sodium solutions of chloride, as well as a 4% sodium solution of bicarbonate. The second reason is the exogenous administration of corticosteroids, in one degree or another with mineralocorticoid properties. Because of the excess of aldosterone, sodium and water is delayed by the kidneys, potassium losses in exchange for sodium. As a result, hypervolemic hypernatremia and hypokalemia are developing.

Diagnosis of hypernatremia
To clarify the mechanisms of hypernatremia, the study of urine osmolalism and sodium content in it is very important.

A little physiology
Urine Opelness, as well as the general osmolality of blood depends on the concentration of sodium, glucose and urea. Unlike the size of the blood osmolality, it varies widely: it may increase (more than 400 mos / kg of water), to be normal (300 - 400 mos / kg of water) and reduced (less than 300 mos / kg of water). In the absence of the possibility of measuring urine osmolality for an approximate estimate, the value of the proportion of urine can be used.

The combination of high urine osmolality and hypernatremia indicates possible three states:

Dehydration and reduced water intake (hypodipsy),
excess mineralocorticoids,
Solving exogenous sodium administration.

For the differential diagnosis of these states, the study of sodium content in the urine is useful. Sodium concentration in the urine is low during dehydration and other non-performing causes of hypernatremia, high - with an excess of mineralocorticoids and exogenous administration of sodium.

Normal urine osmolalism and hypernatremia are noted when using diuretics, with a non-warning diabetes. Low urine osmolability and hypernatremia indicates a serious central or nephrogenic non-car diabetes. Sodium content in the urine in all these cases is variable.

Hyponatremia
Hyponatremia is not an early symptom at CMT. Its development, as a rule, is already noted in the conditions of treatment, therefore, with hyponatremia, the volume of circulating blood is almost normal or slightly elevated. In contrast to hypernatremia, which is always accompanied by a hyper-permal state of blood, hyponatremia can be combined with both hyperosmolyness and normo and hyposmolyness.

Hypertensive hyponatremia
Hypertensive hyponatremia is the most rare and least logical form of reducing sodium content in the blood. Sodium levels are reduced - the main agent providing the osmotic properties of blood, and the osmolayality is increased! This type of hyponatremia can only be developed when accumulating in the blood of a significant number of other osmotically active substances - glucose, urea, starch, dextrans, alcohol, mannitol. These agents can be entered from outside or produced endogenously. An example of an endogenous mechanism for the development of hypertensive hyponatremia is hyperglycemia due to decompensation of diabetes. This situation is often found in the elderly patients with CHMT. With increasing blood osmolality in it, the sodium level is reduced. If osmolayality exceeds 295 mosm / kg of water, mechanisms derived sodium from the body are included. As a result, not only sodium concentration in the blood is reduced, but its absolute amount.

Hypo- and normal hyponathemia
Hyborne and normal hyponatremia reflect the different degree of activity of the same pathological processes. In lighter cases, there is no normal alimony. More often, the decrease in the level of sodium in the blood is accompanied by its hyposphate. Five mechanisms can lead to hypotonic hypotonic hypotonic hypoconathemia:

1. Diving intoxication.
2. Sundar redundant ADG generation.
3. Real and cerebral solventing syndromes.
4. Mineralocorticoid failure.
5. Osmostat's Reset (OSMOSTAT'S RESET).

The first two mechanisms cause excess water, the second two are lack of sodium. The last mechanism is most likely reflecting the so-called "stress rate".

Water intoxication
The aqueous intoxication develops more oftenly, as a consequence of inadequate correction of hypovolemia, accompanied by water loss and sodium. An adequate replenishment of water loss and insufficient correction of sodium losses leads to water intoxication. One of the arguments of supporters of restriction of application at CMT solutions of glucose is the development of water intoxication when using these funds. Explanation The following: glucose is metabolized to carbon dioxide and water. As a result, overflowing glucose solutions, only water is in fact injected. As far as this mechanism is important for the development of brain edema and increasing the GFD, it remains unclear.

Excessive Development Syndrome
Syndrome of excessive production ADG, called an even syndrome of inadequate secretion of ADG, leads to a delay in water in the body due to its increased reabsorption in the renal tubules. As a result, the volume of urine and sodium content in the blood is reduced. Despite the hyponatremia, sodium concentration in the urine exceeds 30 MEKV / l due to the compensatory stimulation of the atrial sodium systemic factor and suppressing the secretion of aldosterone.

Solherying syndromes and mineralocorticoid failure
With rear and cerebral soluble syndromes, as well as with mineralocorticoid insufficiency, excessive sodium losses with urine are noted. Their immediate culprit with cerebral solitary syndrome is Wabaive, which enhances the removal of sodium by the kidneys.

The reasons for the development of the renal solventy syndrome most often remain unclear. Perhaps, the preceding kidney diseases or genetic defects with a sensitivity impairment to the PNF and Wabaine are. Excessive sodium loss compared to water loss can be observed when using saluretics. With mineralocorticoid deficiency, the low content of aldosterone causes a disruption of sodium reverse absorption in renal tubules with the development of sodium cutting and hyponatremia.

Osmostat Reset Syndrome (Osmostat's Reset)
In this case, the syndrome on obscure reasons establishes a new normal level of sodium, so the kidneys do not react to this level by compensatory changes in sodium and water release.

Diagnosis of hypotonic hypotonic hyponatremia
For the differential diagnosis of the causes of hypotonic hyponatremia in our clinic, the following algorithm is used (Fig. 3.2). According to this algorithm, in addition to the study of blood osmolality and the level of sodium, the definition of urine osmolality and sodium concentration in it is obligatory. Sometimes for detailing the diagnosis it is necessary to carry out pharmacological samples. In all cases, treatment begins with the introduction of hypertensive (3%) sodium solutions of chloride.

High urine osmolability (more than 400 mos / kg of water) in combination with hyponatremia indicates excessive Development Syndrome. At the same time there is an increase in sodium concentration in the urine - more than 30 MEKV / l. Urine osmolalism remains almost constant with the change in the amount of fluid and the tempo of its administration. This is a very important symptom, since in other cases of hyponatremia infusion load and liquid limit cause corresponding urine osmolalism changes. The introduction of a 3% solution of sodium chloride allows you to temporarily increase the level of sodium in the blood without significantly influence on the sodium content in the urine.

Hyponatremia and low urine osmolability can be combined both low and high sodium levels in the urine. Low sodium level (less than 15 MKV / L) indicates water intoxication or syndrome reinstalling ossemostat. To diagnose water intoxication, it is necessary to conduct a thorough analysis of the clinical picture, the composition of the injected drugs, the study of the kidney function and biochemical blood tests. The diagnosis of water intoxication is made on the basis of the elimination of all possible causes of sodium losses, except for the sodium limit in the diet and in the composition of infusion therapy. For the differential diagnosis between these syndromes, it is necessary to introduce a hypertensive solution of sodium chloride. With aqueous intoxication, this pharmacological sample leads to the restoration of sodium concentration in the blood with a gradual increase in sodium level in the urine.

Gradually normalizes urine osmolability. The introduction of a hypertensive solution of sodium chloride in the syndrome of reinstallation of osmostat has a temporary effect on the level of sodium in the blood. In the urine after this test, transient hypernatremia and hyperosmolability are noted.

Low or normal urine osmolability with a high sodium content in the urine (more than 30 MEKV / L) indicates either soluble syndromes (including due to the use of saluretics), or on mineralocorticoid failure. The introduction of a 3% solution of sodium chloride causes a temporary increase in blood sodium level. Simultaneously increase sodium losses with urine. For the differential diagnosis of mineralocorticoid insufficiency and soluble syndromes, the introduction of preparations with mineralocorticoid effects (for example, floccortisone) is used.

After applying exogenous mineralocorticoids, under mineralocorticoid insufficiency, sodium concentration in the urine decreases and its content in the blood increases, with soluble syndromes, these indicators remain unchanged.

Hypokalemia
A little physiology
For a correct assessment of the causes of hypokalemia, it is necessary to use the Rule of the Gamble and the concept of anionic failure.

According to the range of the gamble, the body always supports blood plasma electronics (Fig. 3.3). In other words, in the blood plasma there must be the same number of oppositely charged particles - anions and cations.

The main plasma cations are sodium and potassium. The main anions are chlorine, bicarbonate and proteins (mostly albumin). In addition, there are many other cations and anions, the concentration of which is difficult to control in clinical practice. The plasma sodium concentration is normal amounts to 140 MEKV / L, potassium - 4.5 MEKV / L, calcium - 5 MEKV / L, magnesium - 1.5 MEKV / L, chlorides - 100 MEKV / L and bicarbonate - 24 MEKV / l. Approximately 15 MEKV / L is provided by the negative charge of albumin (at its normal level). The difference between the content of cations and anions is:
(140 + 4.5 + 5 + 1.5) - (100 + 24 + 15) \u003d 12 (MEKV / L).

The remaining 12 MEKV / L are provided by undefined anions and are called an "anionic failure". Uncertain anions are ions of mineral acids isolated by kidneys (sulfate ion, phosphate ion, etc.). When calculating the values \u200b\u200bof anionic failure, the level of albumin must be taken into account. When a decrease in the level of this protein for every 10 g / l, the charge created by them decreases by 2-2.5 MKV / l. Accordingly, anion failure increases.

The most frequent cause of hypocalemia is hypovolemia. Reducing the volume of circulating blood causes the activation of the aldosterone secretion, which provides a compensatory sodium delay. In order for the sodium delay in the sodium organism, blood plasma was maintained, the kidneys output another cation - potassium (Fig. 3.4).

Another cause of hypokalemia is the herogenous excess of the mineralocorticoid hormone of aldosterone. At CMT, this cause can lead to hypokalemia with an exogenous administration of hydrocortisone, prednisone, dexamethasone and other corticosteroid preparations with mineralocorticoid properties (Fig. 3.5).

Similar mechanisms lead to hypokalemia when using saluretics. Furosemide and other saluretics cause loss of sodium and water by blocking the reabsorption of these substances in the renal tubules. Water loss lead to secondary hyperaldosteroneism, sodium delay and potassium removal (Fig. 3.6).

Another reason for hypokalemia, at CMT, there may be vomiting and constant active aspiration of gastric content by prison (Fig. 3.7). In these cases, hydrochloric acid is lost, that is, hydrogen and chlorine ions, as well as water. Reducing the blood plasma content of each of them can cause hypocalemia by activating various mechanisms.

Water losses induce secondary aldosteronism, and the kidneys compensatoryly delay sodium and remove potassium.
Reducing the concentration of hydrogen ions and chlorine in blood plasma causes hypochlorinemic alkalosis.

Alkalosis is an excess of bicarbonate ions. To compensate for this excess and maintaining a normal pH of the plasma, hydrogen ions are attracted, which come from intracellular space. Instead of lost hydrogen ions, the cells capture potassium from plasma, and it goes into cells. As a result, hypokalemia develops. Metabolic alkalosis and hypokalemia is a very frequent combination, regardless of which of them is the cause, and as a consequence.

Frequently used at CMT β-adrenomimetics also leads to hypokalemia as a result of activation of mechanisms, redistribution of potassium from plasma in a cell (Fig. 3.8).

To clarify the etiology of hypokalemia informative is the study of chlorides in the urine. Their high content (more than 10 MEKV / L) is characteristic of excess mineralocorticoids (hyperaldosteroneism, hypovolemia). Low chloride content (less than 10 MKV / L) is characteristic of other hypokalemia mechanisms.

A little physiology
The main extracellular cation - sodium. The main intracellular cation is potassium. Normal concentration of blood plasma ions: sodium - 135-145 MEKV / L, potassium - 3.5-5.5 MEKV / l. Normal concentrations of ions inside cells: sodium - 13-22 MEKV / L, potassium - 78-112 meq / l. Maintaining the sodium and potassium gradient on both sides of the cell membrane ensures the vital activity of the cell.

This gradient is supported by the work of the potassium-sodium pump. During depolarization of the cell membrane, sodium enters the cell, and the potassium leaves it according to the concentration gradient. Inside the cell, the concentration of potassium decreases, sodium level - rises. Then the level of ions is restored. The potassium-sodium pump "pumps" potassium against the concentration gradient inside the cell, and sodium - "pumps" from it (Fig. 3.9). Due to the fact that in the blood plasma level of potassium low, minor changes in the concentration of this cation are significantly affected at its absolute value. Increased potassium levels in plasma from 3.5 to 5.5 MEKV / L, that is, 2 MEKV / L means an increase of more than 50%. Increasing the concentration of potassium inside the cell from 85 to 87 MEKV / L, that is, the same 2 MEKV / L, constitutes an increase of only 2.5%! It would not be worthwhile to engage in these arithmetic actions, if not a constant confusion with hypokalemia and hypokaligistia in textbooks, journal publications and during professional discussions. Often you can meet the "scientific" reasoning of this kind: "There is no matter how much potassium in plasma is important - what is it in cells!". Not to mention that in clinical practice it is difficult to assess the level of potassium inside the cells, it is fundamentally important to understand that most of the well-known physiological effects of potassium are associated with its content in blood plasma and do not depend on the concentration of this cation in cells.

Hypokalemia leads to the following negative consequences.
The weakness of transverse and striped and smooth muscles is developing. Muscles of legs are the first to suffer, right up to the development of tetraplegia. At the same time, violations of the functions of the respiratory muscles are noted. Even with moderate hypokalemia due to violations of the functions of a smooth muscles, parisis of intestines appears.
The sensitivity of the muscles of the vessels to catecholaminams and angiotensin is worse, as a result of which the adhesion is noted.
The sensitivity of the renal epithelium to ADG is disturbed, which is the development of polyuria and polydipsy.
The very important negative consequence of hypokalemia is to reduce the threshold for the occurrence of ventricular fibrillation and the acceleration of the mechanisms of circulation of the exciting pulse over the conductive heart system - Re-Entry. This leads to an increase in the frequency of the heart arrhythmias, launched by this mechanism. The depression of the ST segment is noted on the ECG, the appearance of teeth U, smoothing and inversion of the teeth (Fig. 3.10). Contrary to common misconception, changes in potassium levels do not significantly affect the frequency of normal (sinus) rhythm.

Long-term maintenance of hypovolemia leads to depletion of not only potassium reserves in the blood, but also in cells, that is, hypokalemia may be accompanied by hypocaligissia. Hypologicity has less obvious negative consequences than hypokalemia. These consequences are not developing for a long time due to large potassium reserves in cells, but in the end, the metabolic processes in the cell are disturbed due to the violations of the potassium-sodium pump.

These pathophysiological mechanisms explain the feeling of "black hole" known to many reanimates, when the daily introduction of large doses of exogenous potassium allows you to maintain the level of potassium in the blood plasma only on the lower boundary of the norm. Exoginably entered potassium is sent to the relief of hypocalagism and need quite a lot of time to fill potassium deficiency in the body. Increasing the rate of administration of exogenous potassium does not allow the specified problem, since the threat of hypercalemia with preserving hypokaligissia arises.

Hypercalemia
Hypercalemia with an isolated CMT arises rarely. Two mechanisms can lead to its development. The first is yathedral. Inefficient attempts to stop hypokalemia can encourage the doctor to excessively increase the rate of administration of potassium-containing solutions. The intracellular sector can accommodate a lot of potassium. But to enter potassium into intracellular space, you need a certain time, so the clinical effects are developing not due to changes in potassium levels in cells, and due to the temporary increase in the content of this ion in the blood plasma.

The second cause of hypercalemia at CMT - kidney damage due to injury, circulatory disorders or the use of nephrotoxic drugs. In this case, hypercalemia is necessarily combined with oliginia and is one of the signs of the true form of acute renal failure.

Clinical manifestations of hypercalemia are mainly associated with impaired heart rate and conductivity. The ECG is noted the expansion of the QRS complex, the narrowing and growth of the teeth T. Intervals PQ and Qt increases (Fig. 3.11). Muscle weakness is noted, as well as arterial hypotension due to peripheral vasodilation and reducing the pump function of the heart.

Other electrolyte violations
Disturbance of calcium, magnesium, phosphates should be assumed when inexplicable neuromuscular disorders occur. Citomagnation is more often observed. In this regard, in violation of nutrition, alcoholism, inflammatory diseases of the intestines and diarrhea, diabetes, the use of a number of drugs (saluretics, digitalis, aminoglycosides), it is necessary to remember the reimbursement of a possible magnesium deficiency.

Electrolytes - substances that allow transfer of electrical impulses. They also perform many other functions, so a special role is played in the human body. There are several essential electrolytes for a person. If their deficit arises, serious problems will appear. Together with the loss of fluid, a person loses and useful salts, so it is important to maintain their quantity in the norm by igniting the lack of or special medicines.

Not all people understand what it is. Under human electrolytes, salts are implied that are capable of carrying out electrical impulses. These substances perform several essential functions, among which there is a transmission of nerve pulses. In addition, they perform the following functions:

• keep the water-salt balance
• regulate important organism systems

Each electrolyte performs its function. Allocate the following types:

• magnesium
• sodium

There are norms of blood electrolytes in the blood. If there is a lack or oversupply of substances, problems arise with the body. Salts affect each other, thereby creating a balance.

Why are they so important?

In addition to the fact that they affect the transmission of nerve impulses, each electrolyte has an individual function. For example, helps in the work of the heart muscle and brain. Sodium helps the muscles of the body respond to nervous impulses and perform their work. The normal amount of chlorine in the body helps the digestive system to function correctly. Calcium affects the strength of bones and teeth.

Based on this, it becomes clear that the electrolytes perform many functions, so it is important to maintain their optimal content in the body. A shortage or excess one of the substances lead to serious pathologies, which in the future lead to health problems.

Electrolytes are stiguously lost with liquid. If a person, he must keep in mind that it will be necessary to fill out not only water, but also salts. There are special drinks that restore water-electrolyte balance in the human body. They are used so that there are no dangerous pathologies due to the loss of large amounts of salts and liquids.

Symptoms of pathology

If there is a deficit or oversupply of electrolytes, it will necessarily affect human health. There will be various symptoms that need to be paid attention to. The deficit occurs due to the large loss of liquids, diseases and irregular nutrition. The overabundance of substances arises due to the use of products that contain salts in large quantities, as well as during the defeats of certain organs of diseases.

If the electrolyte deficit arises, the following symptoms arise:

• weakness
• arrhythmia
• tremor
• drowsiness
• defeat kidney

If these symptoms occur, you need to consult a doctor. To determine the cause of their appearance will help the blood test on electrolytes. With it, it is determined by the number of salts affecting the water and electrolyte balance in the body at the time of delivery of blood.