Brief information about the physiology of water-salt metabolism

9. Basic electrolytes of the body

Physiology of sodium metabolism

The total amount of sodium in the body of an adult is about 3-5 thousand meq (mmol) or 65-80 g (on average 1 g/kg body weight). 40% of all sodium salts are in the bones and do not participate in metabolic processes. About 70% of exchangeable sodium is contained in the extracellular fluid, and the remaining amount is 30% in the cells. Thus, sodium is the main extracellular electrolyte, and its concentration in the extracellular sector is 10 times higher than that in the cellular fluid and averages 142 mmol/l.

Daily balance.

The daily sodium requirement for an adult is 3-4 g (in the form of sodium chloride) or 1.5 mmol/kg body weight (1 mmol Na is contained in 1 ml of 5.85% NaCl solution). Basically, the excretion of sodium salts from the body occurs through the kidneys and depends on factors such as aldosterone secretion, acid-base status and potassium concentration in the blood plasma.

The role of sodium in the human body.

In clinical practice, sodium balance disturbances may occur in the form of its deficiency and excess. Depending on the concomitant disturbance of water balance, sodium deficiency in the body can occur in the form of hypoosmolar dehydration or in the form of hypoosmolar overhydration. On the other hand, excess sodium is combined with an imbalance of water balance in the form of hyperosmolar dehydration or hyperosmolar overhydration.

Potassium metabolism and its disorders

Physiology of potassium metabolism

Potassium content in the human body. A person weighing 70 kg contains 150 g or 3800 mEq/mmol/potassium. 98% of total potassium is found in cells, and 2% is in the extracellular space. 70% of the total potassium in the body is contained in muscles. The concentration of potassium in different cells is not the same. While a muscle cell contains 160 mmol of potassium per 1 kg of water, an erythrocyte contains only 87 mmol per 1 kg of plasma-free erythrocyte sediment.
Its concentration in plasma ranges from 3.8-5.5 mmol/l, averaging 4.5 mmol/l.

Daily potassium balance

The daily requirement is 1 mmol/kg or 1 ml of 7.4% KCl solution per kg per day.

Absorbed with regular food: 2-3 g /52-78 mmol/. Excreted in urine: 2-3 g /52-78 mmol/. 2-5 g /52-130 mmol/ are secreted and reabsorbed in the digestive tract.

Losses in feces: 10 mmol, losses in sweat: traces.

The role of potassium in the human body

Participates in the use of carbons. Necessary for protein synthesis. During protein breakdown, potassium is released, and during protein synthesis, it is bound (ratio: 1 g of nitrogen to 3 mmol of potassium).

Takes a decisive part in neuromuscular excitability. Each muscle cell and each nerve fiber represents, under resting conditions, a kind of potassium “battery”, which is determined by the ratio of extracellular and intracellular potassium concentrations. With a significant increase in the concentration of potassium in the extracellular space (hyperkalemia), the excitability of the nerve and muscle decreases. The excitation process is associated with the rapid transition of sodium from the cellular sector into the fiber and the slow release of potassium from the fiber.

Digitalis preparations cause loss of intracellular potassium. On the other hand, under conditions of potassium deficiency, a stronger effect of cardiac glycosides is noted.

With chronic potassium deficiency, the process of canalicular reabsorption is disrupted.

Thus, potassium takes part in the function of muscles, heart, nervous system, kidneys and even each individual cell of the body.

Effect of pH on plasma potassium concentration

With a normal potassium content in the body, a decrease in pH /acidemia/ is accompanied by an increase in the concentration of potassium in the plasma, and with an increase in pH (alkalemia/) - a decrease.

pH values ​​and corresponding normal plasma potassium values:

pH	7,0	7,1	7,2	7,3	7,4	7,5	7,6	7,7
K +	6,7	6,0	5,3	4,6	4,2	3,7	3,25	2,85	mmol/l

Under conditions of acidosis, an elevated potassium concentration would thus correspond to normal body potassium levels, while normal plasma concentrations would indicate cellular potassium deficiency.

On the other hand, under conditions of alkalosis - with a normal potassium content in the body, a reduced concentration of this electrolyte in the plasma should be expected.

Consequently, knowledge of CBS allows for a better assessment of plasma potassium values.

The influence of cell energy metabolism on potassium concentration inplasma

With the following changes, an increased transition of potassium from cells to the extracellular space (transmineralization) is observed: tissue hypoxia (shock), increased protein breakdown (catabolic states), insufficient carbohydrate intake (diabetes mellitus), hyperosmolar DG.

Increased uptake of potassium by cells occurs when glucose is used by cells under the influence of insulin (treatment of diabetic coma), increased protein synthesis (growth process, administration of anabolic hormones, recovery period after surgery or injury), cellular dehydration.

Effect of sodium metabolism on plasma potassium concentration

With forced administration of sodium, it is intensively exchanged for intracellular potassium ions and leads to leaching of potassium through the kidneys (especially when sodium ions are administered in the form of sodium citrate, and not in the form of sodium chloride, since citrate is easily metabolized in the liver).

Plasma potassium concentrations fall when there is excess sodium as a result of increased extracellular space. On the other hand, sodium deficiency leads to an increase in potassium concentration due to a decrease in the extracellular sector.

Effect of the kidneys on plasma potassium concentration

The kidneys have less influence on the maintenance of potassium reserves in the body than on the maintenance of sodium content. With a deficiency of potassium, therefore, its conservation is only with difficulty possible and therefore, losses may exceed the administered quantities of this electrolyte. On the other hand, excess potassium is easily eliminated with adequate diuresis. With oliguria and anuria, the concentration of potassium in the plasma increases.

Thus, the concentration of potassium in the extracellular space (plasma) is the result of a dynamic balance between its entry into the body, the ability of cells to absorb potassium, taking into account the pH and metabolic state (anabolism and catabolism), renal losses, taking into account sodium metabolism, oxygen metabolism, diuresis, aldosterone secretion , extrarenal losses of potassium, for example, from the gastrointestinal tract.

An increase in plasma potassium concentration is caused by:

Acidemia

Catabolism process

Sodium deficiency

Oliguria, anuria

A decrease in plasma potassium concentration is caused by:

Alkalemia

Anabolism process

Excess sodium

Polyuria

Potassium metabolism disorder

Potassium deficiency

Potassium deficiency is determined by a deficiency of potassium throughout the body as a whole (hypopotassium). At the same time, the concentration of potassium in the plasma (in the extracellular fluid) - potassium plasma, can be reduced, normal or even increased!

In order to replace the loss of cellular potassium, hydrogen and sodium ions diffuse into the cells from the extracellular space, which leads to the development of extracellular alkalosis and intracellular acidosis. Thus, potassium deficiency is closely related to metabolic alkalosis.

Causes:

1. Insufficient intake into the body (norm: 60-80 mmol per day):

Stenoses of the upper digestive tract,

A diet low in potassium and rich in sodium

Parenteral administration of solutions that do not contain potassium or are poor in it,

Anorexia neuropsychiatric,

2. Kidney losses:

A) Adrenal losses:

Hyperaldosteronism after surgery or other trauma,

Cushing's disease, therapeutic use of ACTH, glucocorticoids,

Primary (1st Conn's syndrome) or secondary (2nd Conn's syndrome) aldosteronism (heart failure, cirrhosis of the liver);

B) Renal and other reasons:

Chronic pyelonephritis, renal calcium acidosis,

Stage of polyuria acute renal failure, osmotic diuresis, especially in diabetes mellitus, to a lesser extent with infusion of osmodiuretics,

Administration of diuretics

Alkalosis,

3. Loss through the gastrointestinal tract:

Vomit; biliary, pancreatic, intestinal fistulas; diarrhea; intestinal obstruction; ulcerative colitis;

Laxatives;

Villous tumors of the rectum.

4. Distribution disorders:

Increased uptake of potassium by cells from the extracellular sector, for example, during the synthesis of glycogen and protein, successful treatment of diabetes mellitus, introduction of buffer bases in the treatment of metabolic acidosis;

Increased release of potassium by cells into the extracellular space, for example, during catabolic conditions, and the kidneys quickly remove it.

Clinical signs

Heart: arrhythmia; tachycardia; myocardial damage (possibly with morphological changes: necrosis, fiber ruptures); decrease in blood pressure; ECG abnormality; cardiac arrest (in systole); decreased tolerance to cardiac glycosides.

Skeletal muscles: decreased tone (“muscles are soft, like half-filled rubber heating pads”), weakness of the respiratory muscles (respiratory failure), ascending paralysis of the Landry type.

Gastrointestinal tract: loss of appetite, vomiting, gastric atony, constipation, paralytic intestinal obstruction.

Kidneys: isosthenuria; polyuria, polydipsia; atony of the bladder.

Carbohydrate metabolism: decreased glucose tolerance.

General signs: weakness; apathy or irritability; postoperative psychosis; instability to cold; thirst.

It is important to know the following: potassium increases resistance to cardiac glycosides. With potassium deficiency, paroxysmal atrial tachycardia with variable atrioventricular block is observed. Diuretics contribute to this blockade (additional potassium loss!). In addition, potassium deficiency impairs liver function, especially if there is already liver damage. The synthesis of urea is disrupted, as a result of which less ammonia is neutralized. Thus, symptoms of ammonia intoxication with brain damage may appear.

Diffusion of ammonia into nerve cells is facilitated by concomitant alkalosis. Thus, unlike ammonium (NH4 +), to which cells are relatively impermeable, ammonia (NH3) can penetrate the cell membrane because it is lipid soluble. With an increase in pH (a decrease in the concentration of hydrogen ions (the equilibrium between NH4 + and NH3) shifts in favor of NH3. Diuretics accelerate this process.

It is important to remember the following:

When the synthesis process predominates (growth, recovery period), after leaving the diabetic coma and acidosis, the body's need increases

(of its cells) in potassium. In all states of stress, the ability of tissues to absorb potassium decreases. These features must be taken into account when drawing up a treatment plan.

Diagnostics

To identify potassium deficiency, it is advisable to combine several research methods in order to assess the disorder as clearly as possible.

Anamnesis: It can provide valuable information. It is necessary to find out the reasons for the existing violation. This alone may indicate the presence of potassium deficiency.

Clinical symptoms: Certain signs indicate an existing potassium deficiency. So, you need to think about it if, after surgery, the patient develops atony of the gastrointestinal tract that is not amenable to conventional treatment, unexplained vomiting, an unclear state of general weakness, or a mental disorder occurs.

ECG: Flattening or inversion of the T wave, a decrease in the ST segment, the appearance of a U wave before the T and U merge into a common TU wave. However, these symptoms are not constant and may be absent or not consistent with the severity of potassium deficiency and the degree of kalemia. In addition, ECG changes are not specific and may also be the result of alkalosis and shifts (extracellular fluid pH, cellular energy metabolism, sodium metabolism, renal function). This limits its practical value. In conditions of oliguria, the plasma potassium concentration is often increased, despite its deficiency.

However, in the absence of these influences, it can be assumed that in conditions of hypokalemia above 3 mmol/l, the total potassium deficiency is approximately 100-200 mmol, with potassium concentration below 3 mmol/l - from 200 to 400 mmol, and with its level below 2 mmol/ l - 500 or more mmol.

CBS: Potassium deficiency is usually combined with metabolic alkalosis.

Potassium in urine: its excretion decreases when excretion is less than 25 mmol/day; Potassium deficiency is likely when it decreases to 10 mmol/l. However, when interpreting urinary potassium excretion, it is necessary to take into account the true value of potassium in plasma. Thus, potassium excretion of 30 - 40 mmol/day is high if its plasma level is 2 mmol/l. The potassium content in the urine is increased, despite its deficiency in the body, if the renal tubules are damaged or there is an excess of aldosterone.
Differential diagnostic distinction: in conditions of a diet poor in potassium (starch-containing foods), more than 50 mmol of potassium per day is excreted in the urine in the presence of potassium deficiency of non-renal origin: if potassium excretion exceeds 50 mmol/day, then you need to think about renal causes potassium deficiency.

Potassium balance: Its assessment allows you to quickly find out whether the total potassium content in the body is decreasing or increasing. They should be used as a guide when prescribing treatment. Determination of intracellular potassium content: this is easiest to do in an erythrocyte. However, its potassium content may not reflect changes in all other cells. In addition, it is known that individual cells behave differently in different clinical situations.

Treatment

Taking into account the difficulties of identifying the magnitude of potassium deficiency in the patient’s body, therapy can be carried out as follows:

1. Establish the patient’s need for potassium:

A) provide the normal daily requirement for potassium: 60-80 mmol (1 mmol/kg).

B) eliminate potassium deficiency, measured by its concentration in plasma, for this you can use the following formula:

Potassium deficiency (mmol) = patient weight (kg) x 0.2 x (4.5 - K+ plasma)

This formula does not give us the true value of the total potassium deficiency in the body. However, it can be used in practical work.

C) take into account potassium losses through the gastrointestinal tract
Potassium content in the secretions of the digestive tract: saliva - 40, gastric juice - 10, intestinal juice - 10, pancreatic juice - 5 mmol/l.

During the recovery period after surgery and injury, after successful treatment of dehydration, diabetic coma or acidosis, it is necessary to increase the daily dose of potassium. You should also remember the need to replace potassium losses when using adrenal cortex drugs, laxatives, saluretics (50-100 mmol/day).

2. Choose the route of potassium administration.

If possible, preference should be given to oral administration of potassium supplements. With intravenous administration there is always a danger of a rapid increase in extracellular potassium concentration. This danger is especially great when the volume of extracellular fluid decreases under the influence of massive loss of secretions of the digestive tract, as well as with oliguria.

a) Administration of potassium through the mouth: if the potassium deficiency is not great and, in addition, food intake by mouth is possible, foods rich in potassium are prescribed: chicken and meat broths and decoctions, meat extracts, dried fruits (apricots, plums, peaches), carrots, black radish, tomatoes, dry mushrooms, milk powder).

Administration of potassium chloride solutions. It is more convenient to administer a 1-normal potassium solution (7.45% solution), one ml of which contains 1 mmol of potassium and 1 mmol of chloride.

b) Administration of potassium through a gastric tube: this can be done during tube feeding. It is best to use 7.45% potassium chloride solution.

c) Intravenous administration of potassium: 7.45% potassium chloride solution (sterile!) is added to 400-500 ml of 5%-20% glucose solution in an amount of 20-50 ml. The rate of administration is no more than 20 mmol/h! When the IV infusion rate is more than 20 mmol/h, burning pain appears along the vein and there is a danger of increasing the concentration of potassium in the plasma to a toxic level. It must be emphasized that concentrated solutions of potassium chloride should in no case be administered quickly intravenously in undiluted form! To safely administer a concentrated solution, it is necessary to use a perfuser (syringe pump).

Potassium supplementation should continue for at least 3 days after plasma concentrations have reached normal levels and full enteral nutrition has been restored.

Usually up to 150 mmol of potassium is administered per day. The maximum daily dose is 3 mol/kg body weight - this is the maximum ability of cells to capture potassium.

3. Contraindications to infusion of potassium solutions:

a) oliguria and anuria or in cases where diuresis is unknown. In such a situation, potassium-free infusion fluids are first administered until urine output reaches 40-50 ml/h.

B) severe rapid dehydration. Solutions containing potassium begin to be administered only after the body has been given a sufficient amount of water and adequate diuresis has been restored.

c) hyperkalemia.

D) corticoadrenal insufficiency (due to insufficient excretion of potassium from the body)

e) severe acidosis. They must first be eliminated. As acidosis is eliminated, potassium can be administered!

Excess potassium

Excess potassium in the body is less common than its deficiency, and is a very dangerous condition that requires emergency measures to eliminate it. In all cases, excess potassium is relative and depends on its transfer from cells to blood, although in general the amount of potassium in the body may be normal or even reduced! Its concentration in the blood increases, in addition, with insufficient excretion through the kidneys. Thus, excess potassium is observed only in the extracellular fluid and is characterized by hyperkalemia. It means an increase in plasma potassium concentration beyond 5.5 mmol/l at normal pH.

Causes:

1) Excessive intake of potassium into the body, especially with reduced diuresis.

2) Potassium release from cells: respiratory or metabolic acidosis; stress, trauma, burns; dehydration; hemolysis; after the administration of succinylcholine, when muscle twitching appears, there is a short-term rise in potassium in the plasma, which can cause signs of potassium intoxication in a patient with existing hyperkalemia.

3) Insufficient excretion of potassium by the kidneys: acute renal failure and chronic renal failure; corticoadrenal insufficiency; Addison's disease.

Important: Do not assume an increase in potassium levels duringazotemia, equating it to renal failure. Shouldfocus on the amount of urine or the presence of losses of othersfluids (from a nasogastric tube, through drainages, fistulas) - withpreserved diuresis or other losses, potassium is intensively excreted frombody!

Clinical picture: it is directly caused by an increase in plasma potassium levels - hyperkalemia.

Gastrointestinal tract: vomiting, spasm, diarrhea.

Heart: the first sign is arrhythmia, followed by ventricular rhythm; later - ventricular fibrillation, cardiac arrest in diastole.

Kidneys: oliguria, anuria.

Nervous system: paresthesia, flaccid paralysis, muscle twitching.

General signs: general lethargy, confusion.

Diagnostics

Anamnesis: When oliguria and anuria appear, it is necessary to think about the possibility of developing hyperkalemia.

Clinic details: Clinical symptoms are not typical. Cardiac abnormalities indicate hyperkalemia.

ECG: Tall, sharp T wave with a narrow base; expansion by expansion; the initial segment of the segment is below the isoelectric line, a slow rise with a picture reminiscent of right bundle branch block; atrioventricular nodal rhythm, extrasystole or other rhythm disturbances.

Lab tests: Determination of potassium concentration in plasma. This value is critical, since the toxic effect largely depends on the concentration of potassium in the plasma.

Potassium concentration above 6.5 mmol/l is DANGEROUS, and within 10 -12 mmol/l - DEADLY!

Magnesium metabolism

Physiology of magnesium metabolism.

Magnesium, being part of coenzymes, influences many metabolic processes, participating in enzymatic reactions of aerobic and anaerobic glycolysis and activating almost all enzymes in the reactions of transfer of phosphate groups between ATP and ADP, promoting more efficient use of oxygen and accumulation of energy in the cell. Magnesium ions are involved in the activation and inhibition of the cAMP system, phosphatases, enolases and some peptidases, in maintaining the reserves of purine and pyrimidine nucleotides necessary for the synthesis of DNA and RNA, protein molecules, and thereby influence the regulation of cell growth and cell regeneration. Magnesium ions, activating ATPase of the cell membrane, promote the flow of potassium from the extracellular into the intracellular space and reduce the permeability of cell membranes for the release of potassium from the cell, participate in reactions of complement activation, fibrinolysis of the fibrin clot.

Magnesium, having an antagonistic effect on many calcium-dependent processes, is important in the regulation of intracellular metabolism.

Magnesium, weakening the contractile properties of smooth muscles, dilates blood vessels, inhibits the excitability of the sinus node of the heart and the conduction of electrical impulses in the atria, prevents the interaction of actin with myosin and, thereby, ensures diastolic relaxation of the myocardium, inhibits the transmission of electrical impulses in the neuromuscular synapse, causing curare-like effect, has a narcotic effect on the central nervous system, which is relieved by analeptics (cordiamin). In the brain, magnesium is an essential participant in the synthesis of all neuropeptides known today.

Daily balance

The daily requirement for magnesium for a healthy adult is 7.3-10.4 mmol or 0.2 mmol/kg. Normal plasma concentration of magnesium is 0.8-1.0 mmol/l, 55-70% of which is in ionized form.

Hypomagnesemia

Hypomagnesemia manifests itself when the plasma magnesium concentration decreases below 0.8 mmol/l.

Causes:

1. insufficient intake of magnesium from food;

2. chronic poisoning with barium salts, mercury, arsenic, systematic intake of alcohol (impaired absorption of magnesium in the gastrointestinal tract);

3. loss of magnesium from the body (vomiting, diarrhea, peritonitis, pancreatitis, prescription of diuretics without correction of electrolyte losses, stress);

4. increasing the body’s need for magnesium (pregnancy, physical and mental stress);

5. thyrotoxicosis, dysfunction of the parathyroid gland, cirrhosis of the liver;

6. therapy with glycosides, loop diuretics, aminoglycosides.

Diagnosis of hypomagnesemia

Diagnosis of hypomagnesemia is based on medical history, diagnosis of the underlying disease and concomitant pathology, and laboratory test results.

Hypomagnesemia is considered proven if, simultaneously with hypomagnesemia in the patient’s daily urine, the concentration of magnesium is below 1.5 mmol/l or after an intravenous infusion of 15-20 mmol (15-20 ml of 25% solution) magnesium in the next 16 hours, less than 70% is excreted in the urine. administered magnesium.

Hypomagnesemia Clinic

Clinical symptoms of hypomagnesemia develop when the plasma magnesium concentration decreases below 0.5 mmol/l.

The following are distinguished: forms of hypomagnesemia.

The cerebral (depressive, epileptic) form is manifested by a feeling of heaviness in the head, headache, dizziness, bad mood, increased excitability, internal tremors, fear, depression, hypoventilation, hyperreflexia, positive Chvostek and Trousseau symptoms.

The vascular angina form is characterized by cardialgia, tachycardia, cardiac arrhythmia, and hypotension. The ECG shows a decrease in voltage, bigeminy, negative T wave, and ventricular fibrillation.

With moderate magnesium deficiency, patients with arterial hypertension more often develop crises.

The muscular-tetanic form is characterized by tremor, night spasms of the calf muscles, hyperreflexia (Trousseau, Chvostek syndrome), muscle cramps, and paresthesia. When the level of magnesium decreases to less than 0.3 mmol/l, muscle spasms occur in the neck, back, face (“fish mouth”), lower (sole, foot, fingers) and upper (“obstetrician’s hand”) extremities.

The visceral form is manifested by laryngo- and bronchospasm, cardiospasm, spasm of the sphincter of Oddi, anus, and urethra. Disorders of the digestive tract: decreased and lack of appetite due to impaired taste and olfactory perceptions (cacosmia).

Treatment of hypomagnesemia

Hypomagnesemia can be easily corrected by intravenous administration of solutions containing magnesium - magnesium sulfate, panangin, potassium-magnesium aspartate or by the administration of enteral cobidex, magnerot, asparkam, panangin.

For intravenous administration, a 25% solution of magnesium sulfate is most often used in a volume of up to 140 ml per day (1 ml of magnesium sulfate contains 1 mmol of magnesium).

In cases of convulsive syndrome with unknown etiology, in emergency cases, intravenous administration of 5-10 ml of a 25% solution of magnesium sulfate in combination with 2-5 ml of a 10% solution of calcium chloride is recommended as a diagnostic test and to obtain a therapeutic effect. This allows you to stop and thereby eliminate seizures associated with hypomagnesemia.

In obstetric practice, with the development of convulsive syndrome associated with eclampsia, 6 g of magnesium sulfate is administered intravenously slowly over 15-20 minutes. Subsequently, the maintenance dose of magnesium is 2 g/hour. If the convulsive syndrome does not stop, re-introduce 2-4 g of magnesium over 5 minutes. If seizures recur, it is recommended to put the patient under anesthesia using muscle relaxants, perform tracheal intubation and perform mechanical ventilation.

For arterial hypertension, magnesium therapy remains an effective method of normalizing blood pressure even with resistance to other drugs. Having a sedative effect, magnesium also eliminates the emotional background, which is usually the trigger for a crisis.

It is important that after adequate magnesium therapy (up to 50 ml 25% per day for 2-3 days), normal blood pressure levels are maintained for quite a long time.

During magnesium therapy, it is necessary to carefully monitor the patient’s condition, including assessing the degree of inhibition of the knee reflex, as an indirect reflection of the level of magnesium in the blood, respiratory rate, mean arterial pressure, and diuresis rate. In case of complete suppression of the knee reflex, development of bradypnea, or decreased diuresis, the administration of magnesium sulfate is stopped.

For ventricular tachycardia and ventricular fibrillation associated with magnesium deficiency, the dose of magnesium sulfate is 1-2 g, which is administered diluted in 100 ml of 5% glucose solution for 2-3 minutes. In less emergency cases, the solution is administered over 5-60 minutes, and the maintenance dose is 0.5-1.0 g/hour for 24 hours.

Hypermagnesemia

Hypermagnesemia (an increase in the concentration of magnesium in the blood plasma by more than 1.2 mmol/l) develops with renal failure, diabetic ketoacidosis, excessive administration of drugs containing magnesium, and a sharp increase in catabolism.

Hypermagnesemia clinic.

Symptoms of hypermagnesemia are few and variable.

Psychoneurological symptoms: increasing depression, drowsiness, lethargy. At a magnesium level of up to 4.17 mmol/l, superficial anesthesia develops, and at a level of 8.33 mmol/l, deep anesthesia develops. Respiratory arrest occurs when the magnesium concentration increases to 11.5-14.5 mmol/l.

Neuromuscular symptoms: muscle asthenia and relaxation, which are potentiated by anesthetics and eliminated by analeptics. Ataxia, weakness, decreased tendon reflexes are relieved with anticholinesterase drugs.

Cardiovascular disorders: at a plasma magnesium concentration of 1.55-2.5 mmol/l, the excitability of the sinus node is inhibited and the conduction of impulses in the conduction system of the heart slows down, which is manifested on the ECG by bradycardia, an increase in the P-Q interval, widening of the QRS complex, impaired contractility myocardium. The decrease in blood pressure occurs mainly due to diastolic and to a lesser extent systolic pressure. With hypermagnesemia of 7.5 mmol/l or more, asystole may develop in the diastole phase.

Gastrointestinal disorders: nausea, abdominal pain, vomiting, diarrhea.

The toxic manifestations of hypermagnesemia are potentiated by B-blockers, aminoglycosides, riboxin, adrenaline, glucocorticoids, and heparin.

Diagnostics hypermagnesemia is based on the same principles as the diagnosis of hypomagnesemia.

Treatment of hypermagnesemia.

1. Elimination of the cause and treatment of the underlying disease that caused hypermagnesemia (renal failure, diabetic ketoacidosis);

2. Monitoring of respiration, blood circulation and timely correction of their disorders (oxygen inhalation, auxiliary and artificial ventilation, administration of sodium bicarbonate solution, cordiamine, proserine);

3. Intravenous slow administration of a solution of calcium chloride (5-10 ml of 10% CaCl), which is a magnesium antagonist;

4. Correction of water and electrolyte disorders;

5. If there is a high level of magnesium in the blood, hemodialysis is indicated.

Chlorine metabolism disorder

Chlorine is one of the main (along with sodium) plasma ions. Chlorine ions account for 100 mOsm or 34.5% of plasma osmolarity. Together with sodium, potassium and calcium cations, chlorine participates in the creation of resting potentials and action potentials of membranes of excitable cells. Chlorine anion plays a significant role in maintaining the blood hemoglobin buffer system (hemoglobin buffer system of erythrocytes), the diuretic function of the kidneys, and the synthesis of hydrochloric acid by the parietal cells of the gastric mucosa. In digestion, HCl of gastric juice creates optimal acidity for the action of pepsin and is a stimulator for the secretion of pancreatic juice by the pancreas.

The normal concentration of chlorine in blood plasma is 100 mmol/l.

Hypochloremia

Hypochloremia occurs when the concentration of chlorine in the blood plasma is below 98 mmol/l.

Causes of hypochloremia.

1. Loss of gastric and intestinal juices due to various diseases (intoxication, intestinal obstruction, stenosis of the gastric outlet, severe diarrhea);

2. Loss of digestive juices into the lumen of the gastrointestinal tract (intestinal paresis, thrombosis of the mesenteric arteries);

3. Uncontrolled diuretic therapy;

4. Violation of CBS (metabolic alkalosis);

5. Plasmodulation.

Diagnosis of hypochloremia based on:

1. Based on medical history and clinical symptoms;

2. On the diagnosis of the disease and concomitant pathology;

3. Based on the data of a laboratory examination of the patient.

The main criterion for making a diagnosis and the degree of hypochloremia is determining the concentration of chlorine in the blood and the daily amount of urine.

Clinic of hypochloremia.

The clinical picture of hypochloremia is nonspecific. It is impossible to separate the symptoms of a decrease in plasma chlorine from a simultaneous change in the concentration of sodium and potassium, which are closely interrelated. The clinical picture resembles a state of hypokalemic alkalosis. Patients complain of weakness, lethargy, drowsiness, loss of appetite, nausea, vomiting, sometimes muscle cramps, cramping abdominal pain, intestinal paresis. Symptoms of dyshydria are often associated as a result of fluid loss or excess water during plasmodilution.

Treatment of hyperchloremia consists of carrying out forced diuresis for hyperhydration and using glucose solutions for hypertensive dehydration.

Calcium metabolism

The biological effects of calcium are associated with its ionized form, which, along with sodium and potassium ions, is involved in the depolarization and repolarization of excitable membranes, in synaptic transmission of excitation, and also promotes the production of acetylcholine in neuromuscular synapses.

Calcium is an essential component in the process of excitation and contraction of the myocardium, striated muscles and nasty muscle cells of blood vessels and intestines. Distributed over the surface of the cell membrane, calcium reduces the permeability, excitability and conductivity of the cell membrane. Ionized calcium, reducing vascular permeability and preventing the penetration of the liquid part of the blood into the tissue, promotes the outflow of fluid from the tissue into the blood and thereby has an anti-edematous effect. By enhancing the function of the adrenal medulla, calcium increases the level of adrenaline in the blood, which counteracts the effects of histamine released from mast cells during allergic reactions.

Calcium ions participate in the cascade of blood coagulation reactions, are necessary for the fixation of vitamin K-dependent factors (II, VII, IX, X) to phospholipids, the formation of a complex between factor VIII and von Willebrandt factor, the manifestation of the enzymatic activity of factor XIIIa, and are a catalyst for the processes of conversion of prothrombin into thrombin, retraction of coagulation thrombus.

The calcium requirement is 0.5 mmol per day. The concentration of total calcium in plasma is 2.1-2.6 mmol/l, ionized calcium - 0.84-1.26 mmol/l.

Hypocalcemia

Hypocalcemia develops when the level of total plasma calcium decreases to less than 2.1 mmol/L or when ionized calcium decreases below 0.84 mmol/L.

Causes of hypocalcemia.

1. Insufficient calcium intake due to impaired absorption in the intestines (acute pancreatitis), during fasting, extensive intestinal resections, impaired fat absorption (acholia, diarrhea);

2. Significant losses of calcium in the form of salts during acidosis (with urine) or alkolosis (with feces), with diarrhea, bleeding, hypo- and adynamia, kidney disease, when prescribing medications (glucocorticoids);

3. A significant increase in the body’s need for calcium during the infusion of a large amount of donor blood stabilized with sodium citrate (sodium citrate binds ionized calcium), with endogenous intoxication, shock, chronic sepsis, status asthmaticus, allergic reactions;

4. Disturbance of calcium metabolism as a result of insufficiency of the parathyroid glands (spasmophilia, tetany).

Clinic of hypocalcemia.

Patients complain of constant or recurrent headaches, often of a migraine nature, general weakness, hyper- or paresthesia.

On examination, there is an increase in the excitability of the nervous and muscular systems, hyperreflexia in the form of sharp muscle soreness, tonic contraction: a typical position of the hand in the form of an “obstetrician’s hand” or a paw (the arm bent at the elbow and brought to the body), spasms of the facial muscles (“fish mouth”) "). Convulsive syndrome can turn into a state of decreased muscle tone, even to atony.

On the part of the cardiovascular system, there is an increase in myocardial excitability (increased heart rate to paroxysmal tachycardia). The progression of hypocalcemia leads to a decrease in myocardial excitability, sometimes to asystole. On the ECG, the Q-T and S-T intervals lengthen with normal T wave width.

Severe hypocalcemia causes peripheral circulatory disorders: slowing blood clotting, increasing membrane permeability, which causes activation of inflammatory processes and contributes to a predisposition to allergic reactions.

Hypocalcemia can be manifested by an increased effect of potassium, sodium, and magnesium ions, since calcium is an antagonist of these cations.

With chronic hypocalcemia, the skin of patients is dry, easily cracked, hair falls out, nails are layered with whitish stripes. Bone tissue regeneration in these patients is slow, osteoporosis and increased dental caries often occur.

Diagnosis of hypocalcemia.

Diagnosis of hypocalcemia is based on the clinical picture and laboratory data.

Clinical diagnosis is often situational in nature, since hypocalcemia is most likely to occur in situations such as blood or albumin infusion, administration of saluretics, and hemodilution.

Laboratory diagnostics is based on determining the level of calcium, total protein or plasma albumin with subsequent calculation of the concentration of ionized plasma calcium using the formulas: With intravenous administration of calcium, bradycardia may develop, and with rapid administration, while taking glycosides, ischemia, myocardial hypoxia, hypokalemia may occur, ventricular fibrillation, asystole, cardiac arrest in the systole phase. The administration of calcium solutions intravenously causes a feeling of heat, first in the mouth, and then throughout the body.

If a calcium solution is accidentally injected subcutaneously or intramuscularly, severe pain, tissue irritation followed by necrosis occurs. To relieve pain and prevent the development of necrosis, a 0.25% solution of novocaine should be injected into the area of ​​contact with the calcium solution (depending on the dose, the injection volume is from 20 to 100 ml).

Correction of ionized calcium in the blood plasma is necessary for patients whose initial plasma protein concentration is below 40 g/l and who are receiving an infusion of an albumin solution to correct hypoproteinemia.

In such cases, it is recommended to administer 0.02 mmol of calcium for every 1 g/l of infused albumin. Example: Plasma albumin - 28 g/l, total calcium - 2.07 mmol/l. The volume of albumin to restore its level in plasma: 40-28 = 12 g/l. To correct plasma calcium concentration, it is necessary to introduce 0.24 mmol Ca2+ (0.02 * 0.12 = 0.24 mmol Ca2+ or 6 ml of 10% CaCl). After administration of this dose, the plasma calcium concentration will be 2.31 mmol/l.
Clinic of hypercalcemia.

The primary signs of hypercalcemia are complaints of weakness, loss of appetite, vomiting, epigastric and bone pain, and tachycardia.

With gradually increasing hypercalcemia and a calcium level reaching 3.5 mmol/l or more, a hypercalcemic crisis occurs, which can manifest itself in several sets of symptoms.

Neuromuscular symptoms: headache, increasing weakness, disorientation, agitation or lethargy, impaired consciousness to coma.

A complex of cardiovascular symptoms: calcification of the vessels of the heart, aorta, kidneys and other organs, extrasystole, paroxysmal tachycardia. The ECG shows a shortening of the S-T segment; the T wave can be biphasic and begin immediately after the QRS complex.

A complex of abdominal symptoms: vomiting, epigastric pain.

Hypercalcemia more than 3.7 mmol/l is life-threatening for the patient. In this case, uncontrollable vomiting, dehydration, hyperthermia, and coma develop.

Therapy for hypercalcemia.

Correction of acute hypercalcemia includes:

1. Elimination of the cause of hypercalcemia (hypoxia, acidosis, tissue ischemia, arterial hypertension);

2. Protection of the cell cytosol from excess calcium (calcium channel blockers from the verapamine and nifedepine group, which have negative ino- and chronotropic effects);

3. Removal of calcium from urine (saluretics).

Maintaining arterial and venous pressure, the pumping function of the heart, normalizing blood circulation in internal organs and peripheral tissues, regulating homeostasis processes in patients with sudden cessation of blood circulation is impossible without normalization and correction of water and electrolyte balance. From a pathogenetic point of view, these disorders can be the root cause of clinical death and, as a rule, are a complication of the post-resuscitation period. Finding out the causes of these disorders allows us to develop further treatment tactics based on the correction of pathophysiological changes in the exchange of water and electrolytes in the body.

Body water makes up about 60% (55 to 65%) of body weight in men and 50% (45 to 55%) in women. About 40% of the total amount of water is intracellular and intracellular fluid, about 20% is extracellular (extracellular) fluid, 5% of which is plasma, and the rest is interstitial (intercellular) fluid. Transcellular fluid (cerebrospinal fluid, synovial fluid, fluid of the eye, ear, glandular ducts, stomach and intestines) normally makes up no more than 0.5-1% of body weight. Secretion and reabsorption of fluid are balanced.

Intracellular and extracellular fluids are in constant equilibrium due to the preservation of their osmolarity. The concept of “osmolarity,” which is expressed in osmoles or milliosmoles, includes the osmotic activity of substances, which determines their ability to maintain osmotic pressure in solutions. This takes into account the number of molecules of both non-dissociating substances (for example, glucose, urea), and the number of positive and negative ions of dissociating compounds (for example, sodium chloride). Therefore, 1 osmol of glucose is equal to 1 gram molecule, while 1 gram molecule of sodium chloride is equal to 2 osmoles. Divalent ions, such as calcium ions, although they form two equivalents (electrical charges), give only 1 osmol in solution.

The unit "mole" corresponds to the atomic or molecular mass of elements and represents the standard number of particles (atoms for elements, molecules for compounds), expressed by Avogadro's number. To convert the amount of elements, substances, compounds into moles, it is necessary to divide the number of grams by their atomic or molecular mass. So, 360 g of glucose gives 2 moles (360: 180, where 180 is the molecular weight of glucose).

A molar solution corresponds to 1 mole of a substance in 1 liter. Solutions of the same molarity can be isotonic only in the presence of non-dissociating substances. Dissociating agents increase osmolarity in proportion to the dissociation of each molecule. For example, 10 mmol of urea in 1 liter is isotonic with 10 mmol of glucose in 1 liter. At the same time, the osmotic pressure of 10 mmol of calcium chloride is equal to 30 mOsm/l, since the calcium chloride molecule dissociates into one calcium ion and two chlorine ions.

Normally, plasma osmolarity is 285-295 mOsm/L, with sodium accounting for 50% of the osmotic pressure of the extracellular fluid, and in general, electrolytes provide 98% of its osmolarity. The main ion of the cell is potassium. Cellular permeability of sodium, compared to potassium, is sharply reduced (10-20 times less) and is caused by the main regulatory mechanism of ionic equilibrium - the “sodium pump”, which promotes the active movement of potassium into the cell and the expulsion of sodium from the cell. Due to disturbances in cell metabolism (hypoxia, exposure to cytotoxic substances or other causes contributing to metabolic disorders), pronounced changes in the function of the “sodium pump” occur. This leads to the movement of water into the cell and its hyperhydration due to a sharp increase in the intracellular concentration of sodium, and then chlorine.

Currently, it is possible to regulate water and electrolyte disturbances only by changing the volume and composition of the extracellular fluid. And since there is an equilibrium between the extracellular and intracellular fluid, it is possible to indirectly influence the cellular sector. The main regulatory mechanism for the constancy of osmotic pressure in the extracellular space is the concentration of sodium and the ability to change its reabsorption, as well as water in the renal tubules.

The loss of extracellular fluid and an increase in plasma osmolarity causes irritation of osmoreceptors located in the hypothalamus and efferent signaling. On the one hand, a feeling of thirst arises, on the other, the release of antidiuretic hormone (ADH) is activated. An increase in ADH production promotes the reabsorption of water in the distal and collecting tubules of the kidneys and the release of concentrated urine with an osmolarity above 1350 mOsm/L. The opposite picture is observed when ADH activity decreases, for example, in diabetes insipidus, when a large amount of urine with low osmolarity is excreted. The adrenal hormone aldosterone increases sodium reabsorption in the renal tubules, but this occurs relatively slowly.

Due to the fact that ADH and aldosterone are inactivated in the liver, during inflammatory and congestive events in the liver, water and sodium retention in the body increases sharply.

The volume of extracellular fluid is closely related to the bcc and is regulated by changes in pressure in the atrial cavities due to irritation of specific volume receptors. Afferent signaling through the regulatory center and then through efferent connections influences the degree of sodium and water reabsorption. There are also a large number of other regulatory mechanisms of water-electrolyte balance, primarily the juxtaglomerular apparatus of the kidneys, baroreceptors of the carotid sinus, the direct blood circulation of the kidneys, the level of renin and angiotensin II.

The body's daily need for water during moderate physical activity is about 1500 ml/sq.m of body surface (for an adult healthy person weighing 70 kg - 2500 ml), including 200 ml of water for endogenous oxidation. At the same time, 1000 ml of fluid is excreted in the urine, 1300 ml through the skin and lungs, and 200 ml in feces. The minimum requirement for exogenous water in a healthy person is at least 1500 ml per day, since at normal body temperature at least 500 ml of urine should be released, 600 ml should evaporate through the skin and 400 ml through the lungs.

In practice, water and electrolyte balance is determined daily by the amount of fluid entering and leaving the body. It is difficult to take into account the loss of water through the skin and lungs. To more accurately determine the water balance, special bed scales are used. To a certain extent, the degree of hydration can be judged by the level of central venous pressure, although its values ​​depend on vascular tone and cardiac performance. However, comparison of indicators of central venous pressure and, to the same extent, APPA, bcc, hematocrit, hemoglobin, total protein, osmolarity of blood plasma and urine, their electrolyte composition, daily fluid balance, along with the clinical picture, makes it possible to determine the degree of disorders of water and electrolyte balance.

In accordance with the osmotic pressure of the blood plasma, dehydration and hyperhydration are distinguished, divided into hypertonic, isotonic and hypotonic.

Hypertensive dehydration(primary dehydration, intracellular dehydration, extracellular-cellular dehydration, water depletion) is associated with insufficient intake of water into the body in patients in an unconscious state, in serious condition, exhausted, elderly people in need of care, with fluid loss in patients with pneumonia, tracheobronchitis, with hyperthermia, profuse sweat, frequent loose stools, with polyuria in patients with diabetes mellitus and diabetes insipidus, with the prescription of large doses of osmotic diuretics.

In the post-resuscitation period, this form of dehydration is most often observed. First, fluid is removed from the extracellular space, the osmotic pressure of the extracellular fluid increases and the concentration of sodium in the blood plasma increases (over 150 mmol/l). In this regard, water from the cells enters the extracellular space and the concentration of fluid inside the cell decreases.

An increase in plasma osmolarity causes an ADH response, which increases the reabsorption of water in the renal tubules. Urine becomes concentrated, with high relative density and osmolarity, and oligoanuria is noted. However, the sodium concentration in it decreases, as aldosterone activity increases and sodium reabsorption increases. This contributes to a further increase in blood plasma osmolarity and worsening cellular dehydration.

At the onset of the disease, circulatory disorders, despite a decrease in central venous pressure and blood volume, do not determine the severity of the patient’s condition. Subsequently, low cardiac output syndrome occurs with a decrease in blood pressure. Along with this, signs of cellular dehydration increase: thirst and dryness of the tongue, mucous membranes of the oral cavity, and pharynx increase, salivation sharply decreases, and the voice becomes hoarse. Laboratory signs, along with hypernatremia, include symptoms of blood thickening (increased hemoglobin, total protein, hematocrit).

Treatment includes ingestion of water (if possible) to replenish its deficiency and intravenous administration of a 5% glucose solution to normalize blood plasma osmolarity. Transfusion of solutions containing sodium is contraindicated. Potassium preparations are prescribed based on its daily requirement (100 mmol) and losses in urine.

It is necessary to differentiate between intracellular dehydration and hypertensive hyperhydration in renal failure, when oligoanuria is also noted and the osmolarity of blood plasma increases. In renal failure, the relative density of urine and its osmolarity are sharply reduced, the concentration of sodium in the urine is increased, and creatinine clearance is low. There are also signs of hypervolemia with a high level of central venous pressure. In these cases, treatment with large doses of diuretics is indicated.

Isotonic (extracellular) dehydration caused by a deficiency of extracellular fluid due to loss of stomach and intestinal contents (vomiting, diarrhea, excretion through fistulas, drainage tubes), retention of isotonic (interstitial) fluid in the intestinal lumen due to intestinal obstruction, peritonitis, copious urine output due to the use of large doses of diuretics, massive wound surfaces, burns, widespread venous thrombosis.

At the beginning of the disease, the osmotic pressure in the extracellular fluid remains constant, there are no signs of cellular dehydration, and symptoms of loss of extracellular fluid predominate. First of all, this is due to a decrease in blood volume and impaired peripheral circulation: severe arterial hypotension is observed, central venous pressure is sharply reduced, cardiac output decreases, and compensatory tachycardia occurs. A decrease in renal blood flow and glomerular filtration causes oligoanuria, protein appears in the urine, and azotemia increases.

Patients become apathetic, lethargic, inhibited, anorexia occurs, nausea and vomiting increase, but there is no pronounced thirst. Skin turgor is reduced, eyeballs lose density.

Laboratory signs include an increase in hematocrit, total blood protein and red blood cell count. The blood sodium level in the initial stages of the disease is not changed, but hypokalemia quickly develops. If the cause of dehydration is the loss of gastric contents, then along with hypokalemia there is a decrease in chloride levels, a compensatory increase in HCO3 ions and the natural development of metabolic alkalosis. With diarrhea and peritonitis, the amount of plasma bicarbonate decreases, and due to peripheral circulatory disorders, signs of metabolic acidosis predominate. In addition, the excretion of sodium and chlorine in urine is reduced.

Treatment should be aimed at replenishing the bcc with a fluid approaching the composition of the interstitial fluid. For this purpose, an isotonic solution of sodium chloride, potassium chloride, plasma and plasma substitutes are prescribed. In the presence of metabolic acidosis, sodium bicarbonate is indicated.

Hypotonic (extracellular) dehydration- one of the final stages of isotonic dehydration if it is not treated correctly with salt-free solutions, for example, 5% glucose solution, or by taking large amounts of liquid orally. It is also observed in cases of drowning in fresh water and excessive gastric lavage with water. At the same time, the sodium concentration in plasma decreases significantly (below 130 mmol/l) and, as a consequence of hypoosmolarity, ADH activity is suppressed. Water is removed from the body, and oligoanuria occurs. Part of the extracellular fluid passes into the cells, where the osmotic concentration is higher, and intracellular hyperhydration develops. Signs of blood thickening progress, its viscosity increases, platelet aggregation occurs, intravascular microthrombi form, and microcirculation is disrupted.

With hypotonic (extracellular) dehydration with intracellular hyperhydration, signs of peripheral circulatory disorders prevail: low blood pressure, a tendency to orthostatic collapse, coldness and cyanosis of the extremities. Due to increased cell edema, phenomena of cerebral, pulmonary edema and, in the terminal stages of the disease, protein-free edema of the subcutaneous tissue may develop.

Treatment should be aimed at correcting sodium deficiency with hypertonic solutions of sodium chloride and sodium bicarbonate, depending on the disturbance of the acid-base state.

In the clinic we most often observe complex forms of dehydration, in particular, hypotonic (extracellular) dehydration with intracellular hyperhydration. In the post-resuscitation period, after a sudden cessation of blood circulation, predominantly hypertonic extracellular and extracellular-cellular dehydration develops. It sharply worsens in severe stages of terminal conditions, with prolonged, treatment-resistant shock, the wrong choice of treatment for dehydration, in conditions of severe tissue hypoxia, accompanied by metabolic acidosis and sodium retention in the body. At the same time, against the background of extracellular dehydration, water and sodium are retained in the interstitial space, which firmly bind to the collagen of the connective tissue. Due to the exclusion of a large amount of water from active circulation, the phenomenon of a decrease in functional extracellular fluid occurs. BCC decreases, signs of tissue hypoxia progress, severe metabolic acidosis develops, and sodium concentration in the body increases.

During an objective examination of patients, noticeable swelling of the subcutaneous tissue, oral mucosa, tongue, conjunctiva, and sclera. Terminal edema of the brain and interstitial tissue of the lungs often develops.

Laboratory signs include a high concentration of sodium in the blood plasma, low protein levels, and an increase in blood urea. In addition, oliguria is observed, and the relative density of urine and its osmolarity remain high. To varying degrees, hypoxemia is accompanied by metabolic acidosis,

Treatment Such disturbances in water-electrolyte balance are a complex and difficult task. First of all, it is necessary to eliminate hypoxemia, metabolic acidosis, and increase the oncotic pressure of blood plasma. Attempts to eliminate edema with the help of diuretics are extremely dangerous for the patient’s life due to increased cellular dehydration and impaired electrolyte metabolism. The administration of a 10% glucose solution with large doses of potassium and insulin (1 unit per 2 g of glucose) is indicated. As a rule, it is necessary to use mechanical ventilation with positive expiratory pressure when pulmonary edema occurs. And only in these cases is the use of diuretics justified (0.04-0.06 g of furosemide intravenously).

The use of osmotic diuretics (mannitol) in the post-resuscitation period, especially for the treatment of pulmonary and cerebral edema, should be treated with extreme caution. With high central venous pressure and pulmonary edema, mannitol increases blood volume and increases interstitial pulmonary edema. In cases of minor cerebral edema, the use of osmotic diuretics may lead to cellular dehydration. In this case, the osmolarity gradient between brain tissue and blood is disrupted and metabolic products in the brain tissue are delayed.

Therefore, for patients with sudden arrest of blood circulation in the post-resuscitation period, complicated by pulmonary and cerebral edema, severe hypoxemia, metabolic acidosis, significant disturbances in water-electrolyte balance (like mixed forms of dyshydria - hypertonic extracellular and extracellular-cellular dehydration with water retention in the interstitial space) it is indicated complex pathogenetic treatment. First of all, patients need mechanical ventilation using volumetric respirators (RO-2, RO-5, RO-6), lowering body temperature to 32-33°C, preventing arterial hypertension, using massive doses of corticosteroids (0 ,1-0.15 g of prednisolone every 6 hours), limiting intravenous fluid administration (no more than 800-1000 ml per day), eliminating sodium salts, increasing the oncotic pressure of blood plasma.

Mannitol should be administered only in cases where the presence of intracranial hypertension is clearly established, and other treatments aimed at eliminating cerebral edema are ineffective. However, a pronounced effect of dehydration therapy in this severe category of patients is extremely rare.

Overhydration in the post-resuscitation period after sudden cessation of blood circulation is observed relatively rarely. It is mainly caused by excessive fluid administration during cardiopulmonary resuscitation.

Depending on the osmolality of the plasma, it is customary to distinguish between hypertonic, isotonic and hypotonic overhydration.

Hyperhydration hypertensive(extracellular saline hypertension) occurs when abundant parenteral and enteral administration of saline solutions (hypertonic and isotonic) to patients with impaired renal excretory function (acute renal failure, postoperative and post-resuscitation period). The concentration of sodium in the blood plasma increases (above 150 mmol/l), water moves from the cells to the extracellular space, and therefore mild cellular dehydration occurs, the intravascular and interstitial sectors increase. Patients experience moderate thirst, anxiety, and sometimes agitation. Hemodynamics remain stable for a long time, but venous pressure increases. Most often, peripheral edema occurs, especially of the lower extremities.

Along with the high concentration of sodium in the blood plasma, the amount of total protein, hemoglobin and red blood cells decreases.

In contrast to hypertensive overhydration, hypertensive dehydration has an increased hematocrit.

Treatment. First of all, you need to stop administering saline solutions, prescribe furosemide (intravenously), protein drugs, and in some cases hemodialysis.

Isotonic hyperhydration develops with abundant administration of isotonic saline solutions in the case of slightly reduced excretory function of the kidneys, as well as with acidosis, intoxication, shock, hypoxia, which increase vascular permeability and promote fluid retention in the interstitial space. Due to an increase in hydrostatic pressure in the venous section of the capillary (heart defects with symptoms of stagnation in the systemic circulation, liver cirrhosis, pyelonephritis), the fluid passes from the intravascular sector to the interstitial sector. This determines the clinical picture of the disease with generalized edema of peripheral tissues and internal organs. In some cases, pulmonary edema occurs.

Treatment consists of using syaluretic drugs, reducing hypoproteinemia, limiting the intake of sodium salts, and correcting complications of the underlying disease.

Hyperhydration hypotonic(cellular hyperhydration) is observed with excessive administration of salt-free solutions, most often glucose, to patients with reduced excretory function of the kidneys. Due to overhydration, the concentration of sodium in the blood plasma decreases (to 135 mmol/l and below), to equalize the gradient of extracellular and cellular osmotic pressure, water penetrates into the cells; the latter lose potassium, which is replaced by sodium and hydrogen ions. This causes cellular hyperhydration and tissue acidosis.

Clinically, hypotonic overhydration is manifested by general weakness, lethargy, convulsions and other neurological symptoms caused by cerebral edema (hypo-osmolar coma).

Of the laboratory signs, noteworthy is a decrease in the concentration of sodium in the blood plasma and a decrease in its osmolality.

Hemodynamic parameters may remain stable, but then CVP increases and bradycardia occurs.

Treatment. First of all, infusions of salt-free solutions are canceled, saluretic drugs and osmotic diuretics are prescribed. Sodium deficiency is eliminated only in cases where its concentration is less than 130 mmol/l, there are no signs of pulmonary edema, and CVP does not exceed normal. Sometimes hemodialysis is necessary.

Electrolyte balance is closely related to water balance and, due to changes in osmotic pressure, regulates fluid shifts in the extracellular and cellular space.

The decisive role here is played by sodium - the main extracellular cation, the concentration of which in the blood plasma is normally approximately 142 mmol/l, and only about 15-20 mmol/l is in the cellular fluid.

Sodium, in addition to regulating water balance, takes an active part in maintaining the acid-base state. With metabolic acidosis, sodium reabsorption in the kidney tubules increases, which binds to HCO3 ions. At the same time, the bicarbonate buffer in the blood increases, and hydrogen ions replaced by sodium are released in the urine. Hyperkalemia interferes with this process, since sodium ions are exchanged mainly for potassium ions, and the release of hydrogen ions is reduced.

It is generally accepted that sodium deficiency should not be corrected in the post-resuscitation period after sudden circulatory arrest. This is due to the fact that both surgical trauma and shock are accompanied by a decrease in sodium excretion in the urine (A. A. Bunyatyan, G. A. Ryabov, A. Z. Manevich, 1977). It must be remembered that hyponatremia is most often relative and is associated with overhydration of the extracellular space, less often with true sodium deficiency. In other words, the patient’s condition should be carefully assessed, based on anamnestic, clinical and biochemical data, the nature of sodium metabolism disorders should be determined and the question of the feasibility of its correction should be decided. Sodium deficiency is calculated using the formula.

Unlike sodium, potassium is the main cation in intracellular fluid, where its concentration ranges from 130 to 150 mmol/l. Most likely, these fluctuations are not true, but are associated with the difficulties of accurately determining the electrolyte in the cells. - The level of potassium in red blood cells can only be determined approximately.

First of all, it is necessary to establish the potassium content in the plasma. A decrease in its concentration below 3.8 mmol/l indicates hypokalemia, and an increase above 5.5 mmol/l indicates hyperkalemia.

Potassium takes an active part in the metabolism of carbohydrates, in the processes of phosphorylation, neuromuscular excitability, and in almost all organs and systems. Potassium metabolism is closely related to the acid-base state. Metabolic acidosis and respiratory acidosis are accompanied by hyperkalemia, since hydrogen ions replace potassium ions in cells and the latter accumulate in the extracellular fluid. The cells of the renal tubules have mechanisms aimed at regulating the acid-base state. One of them is the exchange of sodium with hydrogen and compensation for acidosis. With hyperkalemia, sodium and potassium are exchanged to a greater extent, and hydrogen ions are retained in the body. In other words, with metabolic acidosis, increased excretion of hydrogen ions in the urine leads to hyperkalemia. At the same time, excess intake of potassium into the body causes acidosis.

With alkalosis, potassium ions move from the extracellular to the intracellular space, and hypokalemia develops. Along with this, the excretion of hydrogen ions by renal tubular cells decreases, potassium excretion increases, and hypokalemia progresses.

It should be borne in mind that primary disorders of potassium metabolism lead to serious changes in the acid-base state. Thus, with potassium deficiency due to its loss from both the intracellular and extracellular space, part of the hydrogen ions replaces potassium ions in the cell. Intracellular acidosis and extracellular hypokalemic alkalosis develop. In the cells of the renal tubules, in this case, sodium is exchanged with hydrogen ions, which are excreted in the urine. Paradoxical aciduria occurs. This condition is observed with extrarenal losses of potassium, mainly through the stomach and intestines. With increased excretion of potassium in the urine (hyperfunction of hormones of the adrenal cortex, especially aldosterone, use of diuretics), its reaction is neutral or alkaline, since the excretion of hydrogen ions is not increased.

Hyperkalemia is observed with acidosis, shock, dehydration, acute and chronic renal failure, decreased adrenal function, extensive traumatic injuries and rapid administration of concentrated potassium solutions.

In addition to determining the concentration of potassium in the blood plasma, electrolyte deficiency or excess can be judged by ECG changes. They are more clearly manifested in hyperkalemia: the QRS complex widens, the T wave is high, pointed, the rhythm of the atrioventricular junction, atrioventricular blockade is often recorded, extrasystoles sometimes appear, and with rapid administration of a potassium solution, ventricular fibrillation can occur.

Hypokalemia is characterized by a decrease in the S-T interval below the isoline, widening of the Q-T interval, a flat biphasic or negative T wave, tachycardia, and frequent ventricular extrasystoles. The risk of hypokalemia during treatment with cardiac glycosides increases.

Careful correction of potassium imbalance is necessary, especially after sudden

The daily requirement for potassium varies, ranging from 60 to 100 mmol. The additional dose of potassium is determined by calculation. The resulting solution must be poured at a rate of no more than 80 drops per minute, which is 16 mmol/hour.

For hyperkalemia, a 10% solution of glucose with insulin is administered intravenously (1 unit per 3-4 g of glucose) in order to improve the penetration of extracellular potassium into the cell for its participation in the processes of glycogen synthesis. Since hyperkalemia is accompanied by metabolic acidosis, its correction with sodium bicarbonate is indicated. In addition, diuretics (furosemide intravenously) are used to reduce the level of potassium in the blood plasma, and calcium supplements (calcium gluconate) are used to reduce its effect on the heart.

Disorders of calcium and magnesium metabolism are also important in maintaining electrolyte balance.

Prof. A.I. Gritsyuk

“Correction of water-electrolyte balance disorders during sudden cessation of blood circulation” section Emergency conditions

Additional Information:

• Maintaining adequate blood circulation with correction of blood pressure and pumping function of the heart in case of sudden cessation of blood circulation

Electrolytes play an important role in our water balance and metabolism. Especially during sports and during diarrhea, the body loses a lot of fluid and therefore electrolytes, which must be returned to it to avoid shortages. Find out what foods contain particles and what they cause here.

Staying hydrated is important to prevent electrolyte depletion.

The human body contains more than 60% water. Most of it is found in cells, such as in the blood. There, with the help of electrically charged molecules that are located in cellular fluids, important physiological processes are controlled. Here they play an important role sodium, potassium, chloride, magnesium and calcium. Because of their electrical charge and because they dissolve in intracellular fluid, they are called electrolytes, which means the same as “electric” and “soluble.”

Electrolytes are charged particles that regulate and coordinate important functions in the body. This only works if the fluid balance is correct.

How much water do we need to prevent electrolyte deficiency?

How much fluid a person should take daily is debated over and over again. The Nutrition Society recommends a daily intake of at least 1.5 liters. In addition, there is another liter that we take with us on the road, as well as 350 milliliters (ml) of oxidative water, which is formed during the metabolism of food.

However, water in the body also returns to the environment:

• 150 ml via stool
• 550 ml through the lungs
• 550 ml sweat
• 1600 ml with urine

Excessive sweating, during sports or in the sauna, or diarrheal diseases, provide additional fluid loss. Of course, this must be compensated by increasing fluid intake.

Lack of electrolytes when playing sports?

With liquid, we also lose the minerals it contains, which play an important role in metabolism as electrolytes. To maintain full body functions, these minerals must be returned to the body. This is especially important for athletes because these substances regulate muscles and nerve cells. - an all too familiar symptom. This is why many athletes resort to isotonic drinks.

What role do electrolytes play in diarrhea?

However, large fluid loss occurs not only due to sweating, but also during diarrhea. The fluid in the colon is then barely removed from the chyme, a process by which a healthy person meets most of his fluid needs. The risk of diarrhea is high, especially among children, because they are 70 percent water.

Electrolyte losses must be compensated. One possibility is mineral-fortified drinks. Quick and easy electrolyte solution: Dissolve five teaspoons of glucose and half a teaspoon of table salt in half a liter of water.

What foods contain electrolytes?

Electrolytes come in different forms in many foods and drinks:

Sodium and chloride

This duo is better known as table salt. Important: Too much may negatively affect your The recommended daily dose of six grams should be increased as sweating increases, such as through exercise.

Magnesium

Can magnesium only be taken through effervescent tablets? Wrong! The mineral is present in almost all products. Plant juices often contain magnesium as a dietary supplement. But also in wholemeal products, nuts, legumes and fresh fruits are an energy mineral. often manifests itself in fatigue.

Potassium

Unlike sodium, potassium is barely lost through sweat. However, potassium should be supplemented in cases of severe fluid loss. Wheat bran is valuable, as are legumes, dried fruits and nuts.

Sodium and potassium can hardly be separated from each other from a behavioral point of view. Both play important roles in fluid balance, control muscle contractions, and transmit nerve signals to muscles.

Calcium

The best known sources of calcium are dairy products, especially Parmesan. But lactose intolerant people and vegans can also meet their calcium needs with foods such as fortified soy drinks, fruit juices, bottled water, whole grains, almonds, sesame seeds and green vegetables.

Promotes calcium absorption. The ideal is a combination of fruits and/or vegetables. Calcium, combined with vitamin D, helps build and maintain our bones. Additionally, the mineral—just like magnesium—is important for muscle contraction.

Description:

Hyponatremia - a decrease in sodium concentration in the blood to 135 mmol/l and below, with hypoosmolar and isosmolar hypohydration, means a true Na deficiency in the body. In the case of hypoosmolar overhydration, it may not mean a general sodium deficiency, although in this case it is often observed. (calcium content in the blood is above 2.63 mmol/l).
- decrease in potassium concentration in the blood below 3.5 mmol/l.
- increase in potassium concentration above 5.5 mmol/l.
- decrease in magnesium level below 0.5 mmol/l.

Symptoms:

The clinical picture includes increased neuromuscular excitability, spastic manifestations in the gastrointestinal tract and coronary vessels.

In case of acute calcium poisoning (hypercalcemia), it can develop, which is manifested by acute pain in the epigastrium, thirst, nausea, uncontrollable vomiting, polyuria leading to and then to oligoanuria, hyperthermia, acute circulatory disorders, until it stops.

The main manifestations of hypokalemia: muscle weakness, which can cause hypoventilation, the development of chronic renal failure, decreased tolerance to carbohydrates, dynamic heart rhythm disturbances (fibrillation is possible). On the ECG, the ST interval decreases, RT lengthens, and the T wave flattens. When potassium decreases to 1.5 mmol/l, atrioventricular block develops, and the amplitude of the U wave increases without QT prolongation. Increased sensitivity to cardiac glycosides.

The main clinical manifestations of hyperkalemia: symptoms of neuromuscular damage (weakness, ascending, quadriplegia), intestinal obstruction.

The danger of hyperkalemia is determined by impaired myocardial function. With hyperkalemia of 5–7 mmol/l, the conduction of impulses in the myocardium accelerates; at 8 mmol/l, life-threatening ones occur. The ECG initially shows a tall peaked T wave, followed by prolongation of the PQ interval, disappearance of the P wave, and atrial arrest. Possible widening of the QRS complex, the occurrence of ventricular fibrillation with the development of ventricular fibrillation.
(over 0.75–1 mmol/l) and hypermagnesium histia are observed with a decrease in its excretion by the kidneys, excessive administration, and the use of antacids, especially against the background of chronic renal failure.

Clinical manifestations: with magnesemia 1.25–2.5 mmol/l, nausea, vomiting, feelings of heat and thirst occur. When the concentration exceeds 3.5 mmol/l, drowsiness, hyporeflexia appear, and the conduction of impulses in the myocardium is disrupted. If the magnesium content exceeds 6 mmol/l - coma, respiratory arrest.

Causes:

The main causes of disturbances in water-electrolyte balance are external losses of fluids and pathological redistribution between the main fluid environments.
The main causes of hypocalcemia are:
- trauma to the parathyroid glands;
- radioactive iodine therapy;
- removal of the parathyroid glands;
- .

The most common cause of hypercalcemia is either primary or secondary.

The main causes of hyponatremia include:
- severe debilitating diseases accompanied by decreased diuresis;
- post-traumatic and postoperative conditions;
- extrarenal sodium loss;
- excessive intake of water in the antidiuretic phase of the post-traumatic or postoperative state;
- uncontrolled use of diuretics.

The causes of hypokalemia are:
- displacement of potassium into cells;
- excess potassium losses over its intake is accompanied by hypopotassium histia;
- a combination of the above factors;
- alkalosis (respiratory, metabolic);
- aldosteronism;
- periodic hypokalemic paralysis;
- use of corticosteroids.

The main causes of hyperkalemia are:
- release of potassium from the cell due to its damage;
- potassium retention in the body, most often due to excess intake of catiton into the patient’s body.

The causes of hypomagnesemia may be:

Water-salt metabolism consists of processes that ensure the supply and formation of water and salts in the body, their distribution throughout the internal environment and excretion from the body. The human body consists of 2/3 water - 60-70% of body weight. For men, on average, 61%, for women - 54%. Fluctuations 45-70%. Such differences are mainly due to the unequal amount of fat, which contains little water. Therefore, obese people have less water than thin people and in some cases with severe water obesity can be only about 40%. This is the so-called general water, which is distributed into the following sections:

1. Intracellular water space is the most extensive and makes up 40-45% of body weight.

2. Extracellular water space - 20-25%, which is divided by the vascular wall into 2 sectors: a) intravascular 5% of body weight and b) intercellular (interstitial) 15-20% of body weight.

Water is in 2 states: 1) free 2) bound water, retained by hydrophilic colloids (collagen fibers, loose connective tissue) - in the form of swelling water.

During the day, the human body enters 2-2.5 liters of water with food and drink; about 300 ml of it is formed during the oxidation of food substances (endogenous water).

Water is excreted from the body by the kidneys (approximately 1.5 liters), through evaporation through the skin and lungs, and through feces (in total about 1.0 liters). Thus, under normal (ordinary) conditions, the flow of water into the body is equal to its consumption. This equilibrium state is called water balance. Similar to water balance, the body also needs salt balance.

The water-salt balance is characterized by extreme constancy, since there are a number of regulatory mechanisms that support it. The highest regulator is the thirst center, located in the subcutaneous region. Excretion of water and electrolytes is carried out mainly by the kidneys. In the regulation of this process, two interconnected mechanisms are of paramount importance - the secretion of aldosterone (a hormone of the adrenal cortex) and vasopressin or antidiuretic hormone (the hormone is deposited in the pituitary gland and produced in the hypothalamus). The purpose of these mechanisms is to retain sodium and water in the body. This is done as follows:

1) a decrease in the amount of circulating blood is perceived by volume receptors. They are located in the aorta, carotid arteries, and kidneys. Information is transmitted to the adrenal cortex and the release of aldosterone is stimulated.

2) There is a second way to stimulate this area of ​​the adrenal glands. All diseases in which blood flow in the kidney decreases are accompanied by the production of renin from its (kidney) juxtaglomerular apparatus. Renin, entering the blood, has an enzymatic effect on one of the plasma proteins and splits off a polypeptide from it - angiotensin. The latter acts on the adrenal gland, stimulating the secretion of aldosterone.

3) A 3rd way of stimulating this zone is also possible. In response to a decrease in cardiac output and blood volume, the sympathoadrenal system is activated during stress. In this case, stimulation of b-adrenergic receptors of the juxtaglomerular apparatus of the kidneys stimulates the release of renin, and then through the production of angiotensin and the secretion of aldosterone.

The hormone aldosterone, acting on the distal parts of the kidney, blocks the excretion of NaCl in the urine, while simultaneously removing potassium and hydrogen ions from the body.

Vasopressin secretion increases with a decrease in extracellular fluid or an increase in its osmotic pressure. Osmoreceptors are irritated (they are located in the cytoplasm of the liver, pancreas and other tissues). This leads to the release of vasopressin from the posterior pituitary gland.

Once in the blood, vasopressin acts on the distal tubules and collecting ducts of the kidneys, increasing their permeability to water. Water is retained in the body, and urine output is correspondingly reduced. Little urine is called oliguria.

The secretion of vasopressin can increase (in addition to excitation of osmoreceptors) under stress, pain stimulation, administration of barbiturates, analgesics, especially morphine.

Thus, increased or decreased secretion of vasopressin can lead to retention or loss of water from the body, i.e. water balance may be disrupted. Along with the mechanisms that prevent a decrease in the volume of extracellular fluid, the body has a mechanism represented by Na-uretic hormone, which, released from the atria (apparently from the brain) in response to an increase in the volume of extracellular fluid, blocks the reabsorption of NaCl in the kidneys - those. sodium expelling hormone thereby opposes pathological increase in volume extracellular fluid).

If the intake and formation of water in the body is greater than it is consumed and released, then the balance will be positive.

With a negative water balance, more fluid is consumed and excreted than it enters and is formed in the body. But water with the substances dissolved in it represents a functional unity, i.e. a violation of water metabolism leads to a change in the exchange of electrolytes and, conversely, if there is a violation of the exchange of electrolytes, the exchange of water changes.

Disturbances in water-salt metabolism can occur without a change in the total amount of water in the body, but as a result of the movement of fluid from one sector to another.

Reasons leading to disruption of the distribution of water and electrolytes between the extracellular and cellular sectors

The intersection of fluid between the cell and the interstitium occurs mainly according to the laws of osmosis, i.e. water moves towards a higher osmotic concentration.

Excessive intake of water into the cell: occurs, firstly, when there is a low osmotic concentration in the extracellular space (this can happen with an excess of water and a deficiency of salts), and secondly, when osmosis in the cell itself increases. This is possible if the Na/K pump of the cell is malfunctioning. Na ions are removed from the cell more slowly. The function of the Na/K pump is impaired due to hypoxia, lack of energy for its operation and other reasons.

Excessive movement of water out of the cell occurs only when there is hyperosmosis in the interstitial space. This situation is possible with a lack of water or an excess of urea, glucose and other osmotically active substances.

Reasons leading to disruption of the distribution or exchange of fluid between the intravascular space and the interstitium:

The capillary wall freely allows water, electrolytes and low-molecular substances to pass through, but almost does not allow proteins to pass through. Therefore, the concentration of electrolytes on both sides of the vascular wall is almost the same and does not play a role in the movement of fluid. There is much more protein in the vessels. The osmotic pressure created by them (called oncotic) retains water in the vascular bed. At the arterial end of the capillary, the pressure of moving blood (hydraulic) exceeds the oncotic pressure and water passes from the vessel into the interstitium. At the venous end of the capillary, on the contrary, the hydraulic pressure of the blood will be less than the oncotic pressure and water will be reabsorbed back into the vessels from the interstitium.

A change in these quantities (oncotic, hydraulic pressure) can disrupt the exchange of water between the vessel and the interstitial space.

Disturbances of water and electrolyte metabolism are usually divided into overhydration(water retention in the body) and dehydration (dehydration).

Overhydration observed with excessive introduction of water into the body, as well as with disruption of the excretory function of the kidneys and skin, exchange of water between blood and tissues, and, almost always, with disruption of the regulation of water-electrolyte metabolism. There are extracellular, cellular and general hyperhydration.

Extracellular hyperhydration

It can occur if the body retains water and salts in equivalent quantities. An excess amount of fluid usually does not remain in the blood, but passes into the tissues, primarily into the extracellular environment, which is expressed in the development of hidden or obvious edema. Edema is an excessive accumulation of fluid in a limited area of ​​the body or diffusely throughout the body.

The emergence of both local and and general edema is associated with the participation of the following pathogenetic factors:

1. Increase in hydraulic pressure in the capillaries, especially at the venous end. This can be observed with venous hyperemia, with right ventricular failure, when venous stagnation is especially pronounced, etc.

2. Decrease in oncotic pressure. This is possible with increased protein excretion from the body in urine or feces, reduced protein formation, or insufficient intake of protein into the body (protein starvation). A decrease in oncotic pressure leads to the movement of fluid from the vessels into the interstitium.

3. Increased vascular permeability to protein (capillary wall). This occurs when exposed to biologically active substances: histamine, serotonin, bradykinin, etc. This is possible due to the action of some poisons: bee, snake, etc. The protein enters the extracellular space, increasing the oncotic pressure in it, which retains water.

4. Insufficiency of lymphatic drainage as a result of blockage, compression, spasm of lymphatic vessels. With prolonged lymphatic insufficiency, the accumulation of fluid with a high content of protein and salts in the interstitium stimulates the formation of connective tissue and sclerosis of the organ. Lymphatic edema and the development of sclerosis lead to a persistent increase in the volume of an organ or body part, such as legs. This disease is called "elephantiasis".

Depending on the causes of edema, there are: renal, inflammatory, toxic, lymphogenous, protein-free (cachectic) and other types of edema. Depending on the organ in which the edema occurs, they speak of edema of the pulp, lungs, liver, subcutaneous fat, etc.

Pathogenesis of edema with insufficiency of the right

department of the heart

The right ventricle is not able to pump blood from the vena cava into the pulmonary circulation. This leads to an increase in pressure, especially in the veins of the systemic circle and a decrease in the volume of blood ejected by the left ventricle into the aorta, arterial hypovolemia occurs. In response to this, through stimulation of volume receptors and through the release of renin from the kidneys, the secretion of aldosterone is stimulated, which causes sodium retention in the body. Next, osmoreceptors are excited, vasopressin is released and water is retained in the body.

Since the patient’s pressure in the vena cava (as a result of stagnation) increases, the reabsorption of fluid from the interstitium into the vessels decreases. Lymphatic drainage is also disrupted, because The thoracic lymphatic duct flows into the superior vena cava system, where the pressure is high and this naturally contributes to the accumulation of interstitial fluid.

Subsequently, as a result of prolonged venous stagnation, the patient’s liver function is impaired, protein synthesis decreases, and the oncotic pressure of the blood decreases, which also contributes to the development of edema.

Prolonged venous stagnation leads to liver cirrhosis. In this case, the fluid mainly begins to accumulate in the abdominal organs, from which blood flows through the portal vein. The accumulation of fluid in the abdominal cavity is called ascites. In liver cirrhosis, intrahepatic hemodynamics are disrupted, resulting in stagnation of blood in the portal vein. This leads to an increase in hydraulic pressure at the venous end of the capillaries and limitation of fluid resorption from the interetitium of the abdominal organs.

In addition, the affected liver destroys aldosterone worse, which further retains Na and further disrupts the water-salt balance.

Principles of treatment of edema in right heart failure:

1. Limit the intake of water and sodium chloride into the body.

2. Normalize protein metabolism (parenteral administration of proteins, protein diet).

3. Administration of diuretics that have a sodium-expelling but potassium-sparing effect.

4. Administration of cardiac glycosides (improving heart function).

5. Normalize the hormonal regulation of water-salt metabolism - suppressing the production of aldosterone and prescribing aldosterone antagonists.

6. In case of ascites, the fluid is sometimes removed (the peritoneal wall is pierced with a trocar).

Pathogenesis of pulmonary edema in left heart failure

The left ventricle is unable to pump blood from the pulmonary circulation to the aorta. Venous stagnation develops in the pulmonary circulation, which leads to a decrease in fluid resorption from the interstitium. The patient activates a number of protective mechanisms. If they are insufficient, then an interstitial form of pulmonary edema occurs. If the process progresses, then liquid appears in the lumen of the alveoli - this is an alveolar form of pulmonary edema; the liquid (it contains protein) foams during breathing, fills the airways and disrupts gas exchange.

Principles of therapy:

1) Reduce blood supply to the pulmonary circulation: semi-sitting position, dilation of the systemic vessels: angioblockers, nitroglycerin; bloodletting, etc.

2) Use of antifoam agents (antifomsilan, alcohol).

3) Diuretics.

4) Oxygen therapy.

The greatest danger to the body is swelling of the brain. It can occur due to heat stroke, sunstroke, intoxication (infectious, burn nature), poisoning, etc. Cerebral edema can also occur as a result of hemodynamic disorders in the brain: ischemia, venous hyperemia, stasis, hemorrhage.

Intoxication and hypoxia of brain cells damage the K/Na pump. Na ions are retained in brain cells, their concentration increases, osmotic pressure in the cells increases, which leads to the movement of water from the interstitium into the cells. In addition, if metabolism (metabolism) is disrupted, the formation of endogenous water can sharply increase (up to 10-15 liters). Arises cellular hyperhydration- swelling of brain cells, which leads to an increase in pressure in the cranial cavity and wedging of the brain stem (primarily the oblongata with its vital centers) into the foramen magnum of the occipital bone. As a result of its compression, clinical symptoms such as headache, changes in breathing, cardiac dysfunction, paralysis, etc. can occur.

Correction principles:

1. To remove water from cells, it is necessary to increase the osmotic pressure in the extracellular environment. For this purpose, hypertonic solutions of osmotically active substances (mannitol, urea, glycerin with 10% albumin, etc.) are administered.

2. Remove excess water from the body (diuretics).

General overhydration(water poisoning)

This is an excess accumulation of water in the body with a relative lack of electrolytes. Occurs when a large amount of glucose solutions is administered; with abundant water intake in the postoperative period; when administering Na-free solutions after profuse vomiting or diarrhea; etc.

Patients with this pathology often develop stress, the sympathetic-adrenal system is activated, which leads to the production of renin - angiotensin - aldosterone - vasopressin - water retention. Excess water moves from the blood into the interstitium, lowering its osmotic pressure. Next, water will go into the cell, since the osmotic pressure there will be higher than in the interstitium.

Thus, all sectors have more water and are hydrated, i.e., general hyperhydration occurs. The greatest danger for the patient is overhydration of brain cells (see above).

Basic principles of correction with general overhydration, the same as with cellular hyperhydration.

Dehydration (dehydration)

There are (as well as overhydration) extracellular, cellular and general dehydration.

Extracellular dehydration

develops with the simultaneous loss of water and electrolytes in equivalent quantities: 1) through the gastrointestinal tract (uncontrollable vomiting, profuse diarrhea) 2) through the kidneys (decreased aldosterone production, prescription of sodium-expelling diuretics, etc.) 3) through the skin (massive burns, increased sweating) 4) with blood loss and other disorders.

With the above pathology, first of all, extracellular fluid is lost. Developing extracellular dehydration. Its characteristic symptom is the absence of thirst, despite the serious condition of the patient. The introduction of fresh water is not able to normalize the water balance. The patient's condition may even worsen, because... the introduction of salt-free liquid leads to the development of extracellular hyposmia, and the osmotic pressure in the interstitium drops. Water will move towards a higher osmotic pressure i.e. into cells. In this case, against the background of extracellular dehydration, cellular hyperhydration occurs. Clinically, symptoms of cerebral edema will appear (see above). To correct water-salt metabolism in such patients, glucose solutions cannot be used, because it is quickly recycled and almost pure water remains.

The volume of extracellular fluid can be normalized by administering physiological solutions. The introduction of blood substitutes is recommended.

Another type of dehydration is possible - cellular. It occurs when there is a lack of water in the body, but no loss of electrolytes occurs. Lack of water in the body occurs:

1) when limiting water intake - this is possible when a person is isolated in emergency conditions, for example, in the desert, as well as in seriously ill patients with prolonged depression of consciousness, with rabies accompanied by hydrophobia, etc.

2) A lack of water in the body is also possible with large losses: a) through the lungs, for example, climbers when climbing mountains experience the so-called hyperventilation syndrome (deep, rapid breathing for a long time). Water loss can reach 10 liters. Loss of water is possible b) through the skin - for example, profuse sweating, c) through the kidneys, for example, a decrease in the secretion of vasopressin or its absence (more often with damage to the pituitary gland) leads to increased excretion of urine from the body (up to 30-40 l per day). The disease is called diabetes insipidus, diabetes insipidus. A person is completely dependent on the supply of water from outside. The slightest restriction of fluid intake leads to dehydration.

When the supply of water is limited or its large losses in the blood and in the intercellular space, osmotic pressure increases. Water moves out of cells towards higher osmotic pressure. Cellular dehydration occurs. As a result of stimulation of the osmoreceptors of the hypothalamus and intracellular receptors of the thirst center, a person develops a need to take water (thirst). So, the main symptom that distinguishes cellular dehydration from extracellular dehydration is thirst. Dehydration of brain cells leads to the following neurological symptoms: apathy, drowsiness, hallucinations, impaired consciousness, etc. Correction: it is not advisable to administer saline solutions to such patients. It is better to administer a 5% glucose solution (isotonic) and a sufficient amount of water.

General dehydration

The division into general and cellular dehydration is arbitrary, because all causes that cause cellular dehydration also lead to general dehydration. The clinical picture of general dehydration manifests itself most clearly during complete water fasting. Since the patient also experiences cellular dehydration, the person experiences thirst and actively seeks water. If water does not enter the body, then blood thickening occurs and its viscosity increases. Blood flow becomes slower, microcirculation is disrupted, red blood cells stick together, and peripheral vascular resistance increases sharply. Thus, the activity of the cardiovascular system is disrupted. This leads to 2 important consequences: 1. decreased oxygen delivery to tissues - hypoxia 2. impaired blood filtration in the kidneys.

In response to a decrease in blood pressure and hypoxia, the sympathetic-adrenal system is activated. A large amount of adrenaline and glucocorticoids are released into the blood. Catecholamines enhance the breakdown of glycogen in cells, and glucocorticoids enhance the breakdown of proteins, fats and carbohydrates. Under-oxidized products accumulate in the tissues, the pH shifts to the acidic side, and acidosis occurs. Hypoxia disrupts the potassium-sodium pump, which leads to the release of potassium from the cells. Hyperkalemia occurs. It leads to a further decrease in pressure, a slowdown in heart function and, ultimately, cardiac arrest.

Treatment of the patient should be aimed at restoring the volume of lost fluid. For hyperkalemia, the use of an “artificial kidney” is effective.