Electrolyte balance in the human body. How to recover

Basic physical and chemical concepts:

Osmolarity– a unit of concentration of a substance, reflecting its content in one liter of solvent.

Osmolality– a unit of concentration of a substance, reflecting its content in one kilogram of solvent.

Equivalence– an indicator used in clinical practice to reflect the concentration of substances in dissociated form. Equal to the number of millimoles multiplied by the valence.

Osmotic pressure- the pressure that must be applied to stop the movement of water through a semi-permeable membrane along a concentration gradient.

In the adult human body, water makes up 60% of body weight and is distributed in three main sectors: intracellular, extracellular and intercellular (intestinal mucus, serous fluid, cerebrospinal fluid). The extracellular space includes the intravascular and interstitial compartments. The capacity of the extracellular space is 20% of body weight.

Regulation of the volumes of water sectors is carried out according to the laws of osmosis, where the main role is played by the sodium ion, and the concentration of urea and glucose is also important. Normal blood plasma osmolarity is 282 –295 mOsm/ l. It is calculated according to the formula:

P osm = 2  Na +  +2  TO +  +  Glucose +  urea

The above formula reflects the so-called calculated osmolarity, regulated through the content of the listed components and the amount of water as a solvent.

The term measured osmolarity reflects the actual value determined by the osmometer device. Thus, if the measured osmolarity exceeds the calculated one, then unaccounted for osmotically active substances, such as dextran, ethyl alcohol, methanol, etc., circulate in the blood plasma.

The main ion in extracellular fluid is sodium. Normal concentration in plasma 135-145 mmol/l. 70% of the body's total sodium is intensively involved in metabolic processes and 30% is bound in bone tissue. Most cell membranes are impermeable to sodium. Its gradient is maintained by active removal from cells via Na/K ATPase

In the kidneys, 70% of total sodium is reabsorbed in the proximal tubule and another 5% can be reabsorbed in the distal tubule under the influence of aldosterone.

Normally, the volume of fluid entering the body is equal to the volume of fluid released from it. Daily fluid exchange is 2 - 2.5 liters (Table 1).

Table 1. Approximate daily fluid balance

Water losses increase significantly during hyperthermia (10 ml/kg for each degree above 37 0 C), tachypnea (10 ml/kg at RR  20), and mechanical breathing without humidification.

DYSHYDRIA

Pathophysiology of water metabolism disorders.

Violations can be associated with a lack of fluid (dehydration) or with its excess (overhydration). In turn, each of the above disorders can be isotonic (with normal plasma osmolarity), hypotonic (when plasma osmolarity is reduced) and hypertonic (plasma osmolarity significantly exceeds the permissible normal limits).

Isotonic dehydration - there is both a water deficiency and a salt deficiency. Plasma osmolarity is normal (270-295 mOsm/L). The extracellular space suffers, it is reduced by hypovolemia. It is observed in patients with losses from the gastrointestinal tract (vomiting, diarrhea, fistulas), blood loss, peritonitis and burn disease, polyuria, in case of uncontrolled use of diuretics.

Hypertensive dehydration is a condition characterized by absolute or predominant fluid deficiency with increased plasma osmolarity. Na > 150 mmol/l, plasma osmolarity > 290 mOsm/l. It is observed with insufficient water intake (inadequate tube feeding - 100 ml of water should be administered for every 100 kcal), gastrointestinal diseases, loss of hypotonic fluid - pneumonia, tracheobronchitis, fever, tracheostomy, polyuria, osmodiuresis in diabetes insipidus.

Hypotonic dehydration - there is a water deficiency with a predominant loss of electrolytes. The extracellular space is reduced, and the cells are oversaturated with water. Na<13О ммоль/л, осмолярность плазмы < 275мосм/л. Наблюдается при состояниях, связанных с потерей солей (болезнь Аддисона, применение диуретиков, слабительных, осмодиурез, диета, бедная натрием), при введении избыточного количества инфузионных растворов, не содержащих электролиты (глюкоза, коллоиды).

Water shortage. Water shortages can be caused by either insufficient supply or excessive losses. Lack of intake is quite rare in clinical practice.

Reasons for increasing water losses:

1. Diabetes insipidus

Central

Nephrogenic

2. Excessive sweating

3. Profuse diarrhea

4. Hyperventilation

In this case, it is not pure water that is lost, but hypotonic fluid. An increase in the osmolarity of the extracellular fluid causes intracellular water to move into the vessels, however, this does not completely compensate for the hyperosmolarity, which increases the content of antidiuretic hormone (ADH). Since such dehydration is partially compensated from the intracellular sector, clinical signs will be mild. If the cause is not renal loss, the urine becomes concentrated.

Central diabetes insipidus often occurs after neurosurgery and TBI. The reason is damage to the pituitary gland or hypothalamus, which is expressed in a decrease in the synthesis of ADH. The disease is characterized by polydipsia and polyuria without glugosuria. Urine osmolarity is lower than plasma osmolarity.

Nephrogenic diabetes insipidus develops, most often, secondary to chronic kidney disease and sometimes as a side effect of nephrotoxic drugs (amphotericin B, lithium, demeclocycline, mannitol). The reason lies in a decrease in the sensitivity of renal tubular receptors to vasopressin. The clinical manifestations of the disease are the same, and the diagnosis is verified by the absence of a decrease in the rate of diuresis when ADH is administered.

Sodium deficiency.

The causes of sodium deficiency can be either excessive excretion or insufficient intake. Excretion, in turn, can occur through the kidneys, intestines and skin.

Causes of sodium deficiency:

1. Loss through the kidneys

Polyuric phase of acute renal failure;

Use of diuretics

Mineralocorticoid deficiency

Osmodiuresis (for example, in diabetes mellitus)

2. Loss through the skin

Dermatitis;

Cystic fibrosis.

3. Loss through the intestines

Intestinal obstruction, peritonitis.

4. Loss of fluid rich in salts, compensated by salt-free solutions (profuse diarrhea compensated by 5% glucose solution).

Sodium can be lost in hypo- or isotonic fluids. In both cases, there is a decrease in the volume of extracellular space, which leads to irritation of volume receptors and the release of aldosterone. Increased sodium retention causes an increase in the secretion of protons into the lumen of the nephron tubule and the reabsorption of bicarbonate ions (see renal mechanisms of acid-base regulation), i.e. causes metabolic alkalosis.

When sodium is lost, its concentration in plasma does not reflect the total content in the body, since it depends on the accompanying loss of water. So, if it is lost in the hypotonic fluid, the plasma concentration will be higher than normal; if it is lost in combination with water retention, it will be lower. Loss of equal amounts of sodium and water will not affect its plasma levels. Diagnosis of the predominance of water and sodium losses is presented in Table 2.

Table 2. Diagnosis of predominant water or sodium losses

If water loss predominates, the osmolarity of the extracellular fluid increases, which causes the transition of water from cells to the interstitium and vessels. Therefore, clinical signs will be less clearly expressed.

The most typical case is the loss of sodium in isotonic fluid (isotonic dehydration). Depending on the degree of dehydration of the extracellular sector, three degrees of dehydration are distinguished in the clinical picture (Table 3).

Table 3: Clinical diagnosis of the degree of dehydration.

Excess water.

Excess water is associated with impaired excretion, i.e. renal failure. The ability of healthy kidneys to excrete water is 20 ml/hour, therefore, if their function is not impaired, excess water due to excess intake is practically excluded. Clinical signs of water intoxication are caused primarily by cerebral edema. The danger of its occurrence arises when the sodium concentration approaches 120 mmol/l.

ST. PETERSBURG STATE MEDICAL UNIVERSITY named after. acad. I. P. PAVLOVA

VIOLATIONS

WATER-ELECTROLYTE METABOLISM

AND THEIR PHARMACOLOGICAL CORRECTION

Educational and methodological manual

for students of medical and dental faculties

Saint Petersburg

Doctor of Medical Sciences prof. S. A. Shestakova

Doctor of Medical Sciences prof. A. F. Dolgodvorov

Ph.D. Associate Professor A. N. Kubynin

EDITORS

Doctor of Medical Sciences prof. N. N. Petrishchev

Doctor of Medical Sciences prof. E. E. Zwartau

Disturbances of water-electrolyte metabolism and their pharmacological correction: textbook. manual / ed. prof. N. N. Petrishcheva, prof. E. E. Zwartau. - St. Petersburg. : St. Petersburg State Medical University, 2005. - 91 p.

This educational manual discusses the physiology and pathophysiology of water and electrolyte metabolism. Particular attention is paid to modern ideas about the mechanisms of neurohormonal regulation of water-electrolyte metabolism and their disorders, the causes and mechanisms of typical disorders of water-electrolyte metabolism, their clinical manifestations and the principles of their correction using modern methods and therapeutic agents. The manual includes new information that has appeared in recent years and is not included in the training manuals. The manual is recommended for students of the faculties of medicine and dentistry and is of interest to interns, clinical residents and doctors.

Design and layout:

Panchenko A. V., Shabanova E. Yu.

© St. Petersburg State Medical University Publishing House, 2005.

List of symbols

BP - blood pressure

ADH - antidiuretic hormone

ATP - adenosine triphosphate

ACTH - adrenocorticotropic hormone

ACE - angiotensin-converting enzyme

AP-2 - aquaporin-2

AT - angiotensin

ATPase - adenosine triphosphatase

ACase - adenylate cyclase

BAS - biological active substances

VP - vasopressin

GK - glucocorticosteroids

SMC - smooth muscle cells

DAG - diacylglycerol

Gastrointestinal tract - gastrointestinal tract

IP 3-inositol-3-phosphate

CODE - colloid osmotic (oncotic) pressure

AOS - acid-base state

AKI - acute renal failure

TPR - total peripheral resistance

BCC - circulating blood volume

PG - prostaglandin(s)

PK A - protein kinase A

PC C - protein kinase C

LPO - lipid peroxidation

ANF ​​- atrial natriuretic factor

RAS - renin-angiotensin system

RAAS - renin-angiotensin-aldosterone system

CO - cardiac output

SNS - sympathetic nervous system

STH - somatotropic hormone

FLase - phospholipase

c-AMP - cyclic adenosine monophosphoric acid

CVP - central venous pressure

CNS - central nervous system

COXase - cyclooxygenase

ECG - electrocardiogram

YUGA - juxtaglomerular apparatus

Hb - hemoglobin

Ht - hematocrit

Na+ - sodium

K+ - potassium

Ca 2+ - calcium

Mg 2+ - magnesium

P - phosphorus

List of abbreviations................................................................................................... 3

Introduction.......................................................................................................................... 6

Chapter 1. Content and distribution of water and electrolytes

in the human body........................................................ ........................................................ ... 6

Chapter 2. Body water balance. Stages of water-electrolyte metabolism 11

Chapter 3. Regulation of water-electrolyte metabolism.................................................... 17

Chapter 4. Water metabolism disorders. Causes, mechanisms, manifestations 32

4.1. Dehydration................................................. ................................................... 33

4.1.1. Isoosmolal dehydration................................................................. ......... 33

4.1.2. Hyperosmolal dehydration................................................................. .... 35

4.1.3. Hypoosmolal dehydration................................................................. ...... 38

4.2. Overhydration................................................................... ........................................... 41

4.2.1. Hypoosmolal hyperhydration.................................................................... 42

4.2.2. Hyperosmolal hyperhydration.................................................... 45

4.2.3. Isoosmolal hyperhydration.................................................................... ... 48

4.3. Edema................................................. ........................................................ ................ 50 50

Chapter 5. Disorders of electrolyte metabolism................................................................. .......... 55

5.1. Disorders of sodium metabolism................................................................. ............... 55

5.2. Disorders of potassium metabolism................................................................. ................. 58

5.3. Disorders of calcium metabolism................................................................... ............. 60

5.4. Disorders of phosphorus metabolism................................................................... .......... 64

5.5. Disorders of magnesium metabolism................................................................... ............... 67

Chapter 6. Pharmacological correction of water-electrolyte metabolism disorders 69

6.1. Main directions of infusion therapy.................................................... 70

6.1.1. Restoring adequate bcc (volumetric correction)......... 71

6.1.2. Rehydration and dehydration.................................................................... ............ 72

6.1.2.1. Treatment of dehydration................................................... ............... 72

6.1.2.2. Treatment of overhydration................................................................... .......... 74

6.1.3. Normalization of electrolyte balance and acid-base balance 76

6.1.3.1. Treatment of acid-base disorders......... 76

6.1.3.2. Treatment of electrolyte metabolism disorders.................................... 76

6.1.4. Hemororrheocorrection......................................................... ........................... 79

6.1.5. Detoxification........................................................ ........................................ 80

6.1.6. Exchange-corrective infusions................................................... ........ 80

6.1.7. Other options........................................................ ............................ 81

6.2. Medicines used to correct water-electrolyte imbalance 82

6.2.1. Hemodynamic agents......................................................... ............... 83

6.2.2. Blood-substituting liquids with detoxification action 85

6.2.3. Electrolyte solutions................................................... ................... 86

6.2.4. Preparations for parenteral nutrition.................................................... 88

6.2.5. Exchange corrective solutions................................................... ...... 89

Literature................................................................................................................... 90

INTRODUCTION

The human body, as an open system, is closely connected with its environment, interaction with which is carried out in the form of metabolism.

Both the very existence of the human body and the quality of its life activity depend on the degree of adaptation to changing living conditions. The mechanisms for regulating metabolism, including water and electrolyte metabolism, formed in the process of evolution, are aimed at maintaining the homeostasis of the body and, first of all, the physicochemical parameters of the blood, of which osmolality and proton concentration (pH) are most tightly controlled. Even extreme environmental factors, such as space flight factors, did not change the average values ​​of serum osmolality in astronauts compared to the initial values, despite the increased variability of this indicator after landing (Yu.V. Natochin, 2003).

Such tight control of the osmolality of extracellular fluid (blood) is due to the severe consequences of its change on cell volume due to the movement of water from one water sector to another along the osmolality gradient. A change in cell volume is fraught with significant disturbances in their metabolism, functional state, sensitivity and reactivity to various biological active substances - regulators.

The variety of changes in water-electrolyte metabolism observed in various pathological conditions fits into certain typical disorders, understanding the general patterns of occurrence and development of which is a necessary condition for their effective correction.

CHAPTER 1.

Water is the main substance that makes up the human body. The water content in the body depends on age, gender, and body weight (Table 1). In a healthy adult male weighing 70 kg, the total body water content is about 60% of body weight, i.e. 42 liters. In women, the total amount of water in the body approaches 50% of body weight, i.e. less than in men, which is due to a higher content of water-poor adipose tissue and a lower content of muscle tissue. In a newborn child, the water content in the body reaches 80% of body weight and then gradually decreases with age until old age. This is one of the manifestations of senile involution, depending on changes in the properties of colloidal systems (a decrease in the ability of protein molecules to bind water) and on an age-related decrease in cell mass, mainly muscle tissue. The total water content also depends on body weight: in obese people it is less than in people with normal body weight, and in thin people it is more (Table 1). This is due to the fact that there is significantly less water in adipose tissue than in lean tissue (which does not contain fat).

The deviation of the total water content in the body from the average values ​​within 15% falls within the framework of normal fluctuations.

Table 1. Water content in the body depending on body weight (% of body weight)

Table 2. Water content in various tissues and fluids of the human body

The distribution of water in various human organs and tissues is not the same (Table 2). There is especially a lot of water in cells with a high level of oxidative metabolism, which perform specialized functions and are completely free of fat (their totality constitutes the so-called “cellular mass” of the body).

Water performs important functions in the body. It is an essential component of all cells and tissues and acts as a universal solvent of organic and inorganic substances. Most chemical reactions, i.e., metabolic processes that underlie the life of the body, take place in the aquatic environment. Water is a direct participant in some of them, for example, the hydrolysis of a number of organic substances. It is involved in the transport of substrates necessary for cellular metabolism and the removal of harmful metabolic products from the body. Water determines the physicochemical state of colloidal systems, in particular the dispersion of proteins, which determines their functional characteristics. Since chemical and physicochemical processes in the body are carried out in an aqueous environment that fills the cellular, interstitial and vascular spaces, we can assume that Water is the main component of the internal environment of the body.

All water in the human body is distributed in two main spaces (compartments, sectors, compartments): intracellular (about 2/3 of the total volume of water) and extracellular (about 1/3 of its total volume), separated by plasma membranes of cells (Fig. 1).

Rice. 1. Distribution of water in the body and ways of its entry and exit

Designations: ECF - extracellular fluid; ICF - intracellular fluid; ICF - intercellular (interstitial) fluid; PC - blood plasma; Gastrointestinal tract - gastrointestinal tract

Intracellular fluid makes up 30–40% of body weight, i.e. ~27 l in a man weighing 70 kg, and is the main component of the intracellular space.

Extracellular fluid is divided into several types: interstitial fluid - 15%, intravascular (blood plasma) - up to 5%, transcellular fluid - 0.5–1% of body weight.

Interstitial fluid , surrounding the cells, together with lymph water, makes up about 15–18% of body weight (~11–12 l) and represents the internal environment in which the cells are distributed and on which their vital activity directly depends.

Intravascular fluid , or blood plasma (~3 l), is the medium for the formed elements of blood. In composition, it differs from interstitial fluid in its high protein content (Table 3).

Transcellular fluid located in specialized body cavities and hollow organs (primarily in the gastrointestinal tract) and includes cerebrospinal, intraocular, pleural, intraperitoneal, and synovial fluids; secretions of the gastrointestinal tract, biliary fluid, cavities of the glomerular capsule and kidney tubules (primary urine). These water compartments are separated from the blood plasma by capillary endothelium and a specialized layer of epithelial cells. Although the volume of transcellular fluid is ~1 L, much larger volumes can move into or out of the transcellular space within 24 hours. Thus, the gastrointestinal tract normally secretes and reabsorbs up to 6–8 liters of fluid daily.

In pathology, part of this fluid can be separated into a separate pool of water that does not participate in free exchange (“third space”), for example, exudate accumulated in the serous cavities or sequestered fluid in the gastrointestinal tract during acute intestinal obstruction.

Water compartments differ not only in the quantity, but also in the composition of the liquid they contain. In biological fluids, all salts and most colloids are in a dissociated state, and the sum of cations in them is equal to the sum of anions (law of electrical neutrality).

The concentration of all electrolytes in body fluids can be expressed by the ability of ions to combine with each other depending on the electrical valence - in milliequivalents/liter (meq/l), and in this case the number of cations and anions will be equal (Table 3).

The concentration of electrolytes can be expressed by their mass - in grams or millimoles per liter (g/l, mmol/l). In accordance with the International System of Units (SI), the amount of substances in solutions is usually expressed in mmol/l.

The distribution of electrolytes in various body fluids is characterized by consistency and specificity of composition (Table 3). The ionic composition of intra- and extracellular fluid is different. In the first, the main cation is K +, the amount of which is 40 times greater than in plasma; the predominant anions are phosphate (PO 4 3–) and protein. In the extracellular fluid, the main cation is Na +, the anion is Cl –. The electrolyte composition of blood plasma is similar to that of interstitial fluid, differing only in protein content.

Table 3. Ionic composition and concentration of ions (meq/l) in fluids of various compartments of the human body (D. Sheiman, 1997)

Differences in the electrolyte composition of body fluids are the result of the functioning of active transport processes, selective permeability of barriers between different compartments (the histohematic barrier and cell membranes are freely permeable to water and electrolytes and impermeable to large protein molecules) and cellular metabolism.

Electrolytes and colloids provide an adequate level of osmotic and colloid-osmotic (oncotic) pressure and thereby stabilize the volume and composition of fluid in various water compartments of the body.

Chapter 2.

Body water balance.

Stages of water-electrolyte metabolism

Daily water requirement in a healthy adult, the average is 1.5 liters per unit body surface area (1500 ml/m2) and ranges from a minimum requirement of 700 ml/m2 to a maximum tolerance of 2700 ml/m2. Expressed in relation to body weight, the water requirement is about 40 ml/kg. The fluctuations in water requirements given in the literature (from 1 to 3 l) depend on body weight, age, gender, climatic conditions, and physical activity. An increase in temperature of 1º C is accompanied by an additional fluid requirement of approximately 500 ml/m2 of body surface in 24 hours.

Under normal conditions, the amount of water entering the body is equal to the total amount of water excreted (Table 4). The entry of water into the human body occurs mainly through food and drink. During the process of metabolism, endogenous, or metabolic, water is formed in the body. The oxidation of 100 g of lipids is accompanied by the formation of 107 ml of water, 100 g of carbohydrates - 55 ml, 100 g of proteins - 41 ml of water.

Table 4. Daily water balance of an adult

After absorption in the intestine, water entering the body goes through a certain cycle, entering into processes movements And exchange between sectors of the body, and also participates in metabolic transformations. In this case, the movement of water occurs quite quickly and in large volumes. In a newborn child, about half the volume of extracellular water is exchanged per day, in an adult - about 15%. The entire cycle that the water that enters the body goes through (plasma - cells - biochemical processes - plasma - excretion) takes about 15 days for an adult, 5–6 days for children.

The water compartments in the human body are delimited by semi-permeable membranes, the movement of water through which depends on the difference osmotic pressure on both sides of the membrane. Osmosis- movement of water through a semipermeable membrane from an area of ​​low solute concentration to an area of ​​higher solute concentration. ABOUT smolality- a measure of the ability of a solution to create osmotic pressure, thereby affecting the movement of water. It is determined by the number of osmotically active particles in 1 kg of solvent (water) and is expressed in milliosmoles per kg of water (mosm/kg). In the clinic, it is more convenient to determine the osmotic activity of biological fluids in mOsm/l, which corresponds to the concept osmolarity(Table 5). Since biological fluids are highly diluted, the numerical values ​​of their osmolality and osmolarity are very close.

Table 5. Normal values ​​of osmolarity of human biological fluids

Plasma osmolarity is determined mainly by Na +, Cl – ions and, to a lesser extent, bicarbonate (Table 6).

The part of the osmotic pressure produced in biological fluids by colloids (proteins) is called colloid-osmotic (oncotic) pressure (COD). It accounts for about 0.7% of plasma osmolarity, but is extremely important due to the high hydrophilicity of proteins, especially albumins, and their inability to freely pass through semi-permeable biological membranes.

Effective osmolality, or tonicity, is created by osmotically active substances that are unable to freely penetrate the plasma membranes of cells (glucose, Na +, mannitol).

In the extracellular fluid (plasma), the main osmotically active substances are Na + and Cl – ions; of non-electrolytes - glucose and urea. The remaining osmotically active substances in total provide less than 3% of the total osmolarity (Table 6). Taking this circumstance into account, plasma osmolarity is calculated using the formula

P(mosm/l) = 2´Na + + K + ] + [glucose] + [urea] + 0.03[protein].

The resulting value only approximately corresponds to the true osmolarity, since it does not take into account the contribution of minor plasma components. More accurate data is provided by the cryoscopic method for determining the osmolarity of blood plasma. Normally, the osmotic pressure in all water compartments is approximately the same, so the value of plasma osmolarity gives an idea of ​​the osmolarity of liquids in other water compartments.

Table 6. The content of adult plasma components and their role in the formation of its osmolarity

The plasma osmolality of a healthy person ranges from 280–300 mOsm/kg, which is accepted as the standard of comparison in the clinic. Solutions with tonicity within these limits are called isotonic, for example, 0.9% (0.15 M) NaCl solution. Hypertensive solutions have a tonicity exceeding plasma osmolality (3% NaCl solution) , hypotonic solutions have a tonicity lower than that of plasma (0.45% NaCl solution).

An increase in osmolality in any water sector may be due to an increase in the content of ineffective osmotically active substances (easily passing through a semi-permeable membrane), for example, urea in uremia. However, in this case, urea freely passes into adjacent compartments, and hypertension does not develop in the first compartment. Consequently, there is no movement of water into the first compartment from neighboring ones with the development of dehydration in them.

Thus, the passage of water through the semipermeable plasma membranes of cells is determined by osmotic gradient created by effective osmotically active substances. In this case, the water moves towards a higher concentration until the tonicity of the fluids in the extracellular and intracellular spaces is equal.

Since tonicity determines the direction of water movement, it is obvious that when the tonicity of the extracellular fluid decreases, water moves from the extracellular space to the intracellular space, as a result of which the cell volume will increase (cellular hyperhydration). This occurs when large quantities of distilled water are taken and its excretion is impaired, or when hypotonic solutions are administered during infusion therapy. On the contrary, with an increase in the tonicity of the extracellular fluid, water moves from the cells into the extracellular space, which is accompanied by their wrinkling. This picture is observed due to significant losses of water or hypotonic fluids by the body - for example, with diabetes insipidus, diarrhea, and intense sweating.

Significant changes in cell volume entail disturbances in their metabolism and functions, which are most dangerous in the brain due to the possibility of compression of brain cells located in a strictly limited space, or displacement of the brain when cells shrink. In this regard, the necessary constancy of cell volume is maintained due to the isotonicity of the cytoplasm and interstitial fluid. The existing excess in cells of high molecular weight protein anions and other organic substances that do not freely pass through the membrane is partially balanced by free K + cations, the concentration of which in the cell is higher than outside. However, this does not lead to cellular hyperhydration and subsequent osmotic cell lysis due to the constant work of K + /Na + ATPase, which ensures the removal of Na + from the cell and the return of K + released from it against the cation concentration gradient, for which the cell expends ≈30% of energy . In the event of energy deficiency, insufficiency of the transport mechanism will lead to the entry of Na + and water into the cell and the development of intracellular hyperhydration, observed in the early stage of hypoxia.

Another feature of human cell membranes is the preservation of a potential difference between the cell and the environment equal to 80 mV. The cell membrane potential is determined by the concentration gradient of K + ions (30–40 times more in the cell than outside) and Na + (10 times more in the extracellular fluid than in the cell). Membrane potential is a logarithmic function of the ratio of K +, Na +, Cl – in the intra- and extracellular spaces. If permeability and active transport through the membrane increases, hyperpolarization of the membrane increases, i.e., the accumulation of K + in the cell and the release of Na + from it.

For clinical practice, membrane depolarization is more important. Due to disturbances in active transport and membrane permeability, K + leaves the cell and Na + , H 2 O and H + ions enter the cell, which leads to intracellular acidosis. This is observed in peritonitis, shock, uremia and other severe conditions.

The volume undergoes the greatest fluctuations extracellular fluid which constantly moves between the intravascular and interstitial spaces through diffusion, filtration, reabsorption and pinocytosis through the wall of the exchange vessels. In a healthy person, up to 20 liters of fluid enters the tissues from the vessels per day and the same amount returns back: through the vascular wall - 17 liters and through the lymph - 3 liters.

The exchange of water between the intravascular and interstitial spaces occurs in accordance with E. Starling’s postulate about the balance between hydrostatic and osmotic forces on both sides of the wall of the exchange vessels.

Removing water from the body carried out by a number of physiological systems, of which the leading role belongs to the kidneys.

The formation of final urine involves the processes of ultrafiltration in the glomeruli and reabsorption, secretion and excretion in the tubules. Due to extremely intensive renal perfusion (600 l of blood per day) and selective filtration, 180 l of glomerular ultrafiltrate is formed. In the proximal tubules, an average of 80% of sodium, chloride, potassium and water and almost all glucose, low molecular weight proteins, most amino acids and phosphates are reabsorbed from it. In the loop of Henle and the distal parts of the nephron, the processes of concentration and dilution of urine occur, which is due to the selective permeability of various parts of the loop of Henle and the distal parts of the nephron for sodium and water. The descending limb of the loop of Henle is highly permeable to water and has a relatively low level of active transport and passive permeability for NaCl, which exits into the intercellular space; The ascending limb of the loop of Henle is impermeable to water, but has a high ability to transport Na, Cl, K, Ca from the nephron lumen. This creates a significant corticomedullary osmotic gradient (900 mOsm/L) and a gradient between the contents of the thick ascending limb of the loop of Henle and the surrounding interstitial fluid (200 mOsm/L). Approximately 50% of the osmolality of interstitial fluid is due to the presence of urea in it.

A constant osmotic gradient between the tubular and interstitial fluids causes the release of water from the tubules and increasing concentration of urine towards the papillae of the renal medulla (lower pole of the loop of Henle). In the ascending limb of the loop of Henle, the tubular fluid becomes hypotonic due to the active transport of sodium, chlorine, and potassium from it. In the collecting ducts, ADH-dependent reabsorption of water occurs, concentration and formation of the final urine.

Normally, while ensuring complete elimination of harmful metabolic products, diuresis ranges from 1300 to 1500 per day. The average normal osmolarity of 24-hour urine ranges from 1000 to 1200 mOsm/L, i.e., 3.5–4 times higher than the osmolarity of blood plasma.

If diuresis is< 400 мл/сут, это указывает на oliguria. It occurs when: 1) disruption of the systemic circulation (shock) and renal circulation (renal artery thrombosis); 2) parenchymal renal failure (a significant decrease in the number of functioning renal nephrons with depletion of compensatory mechanisms); 3) disruption of the outflow of urine from the kidneys (renal stone disease).

At polyuria diuresis can reach 20 liters or more (for example, in patients with diabetes insipidus), the relative density of urine and osmolarity are sharply reduced - respectively, no more than 1001 and less than 50 mmol/l. Impaired renal concentrating ability is manifested by a decrease in the relative density of urine and its osmolarity: hyposthenuria- decreased concentrating ability of the kidneys, isosthenuria- a pronounced decrease in it, asthenuria - complete impairment of concentration ability.

Lost Drives perspiration through the skin increase with increased sweating. An increase in body temperature by 1 Cº is accompanied by an increase in water loss by 200 ml or more. During feverish conditions, the body can lose up to 8–10 liters of fluid per day through sweating. Increased water loss through the lungs(with exhaled air) is observed during hyperventilation. Water loss in this way can be very significant in young children when normal nasal breathing is disrupted.

Under normal conditions, from 8–9 liters of fluid entering the gastrointestinal tract per day (saliva - 1500 ml, gastric juice - 2500 ml, bile - 800 ml, pancreatic juice - 700 ml, intestinal juice - 3000 ml) excreted in feces about 100–200 ml of water, the rest of the water is reabsorbed (Fig. 2). Losses of water and electrolytes (K, Cl) through the gastrointestinal tract increase sharply with repeated episodes of vomiting (for example, with toxicosis of pregnancy), with diarrhea (enteritis, intestinal fistulas, etc.), which leads to disturbances in the water-electrolyte balance and CBS (intestinal excretory acidosis). On the contrary, states of reduced intestinal motility may be accompanied by the accumulation in the intestinal lumen of fluid excluded from the general exchange of water (third space).

Rice. 2. Reabsorption of water in the intestine in normal conditions and in diseases

CHAPTER 3.

Date added: 2016-11-23 Types of economic systems (stages of economic development)

Water-electrolyte metabolism is one of the links that ensures the dynamic constancy of the internal environment of the body - homeostasis. Plays an important role in metabolism. The water content in the body reaches 65-70% of body weight. It is customary to divide water into intra- and extracellular. Intracellular water makes up about 72% of all water. Extracellular water is divided into intravascular, circulating in the blood, lymph and cerebrospinal fluid, and interstitial (interstitial), located in the intercellular spaces. Extracellular fluid accounts for about 28%.

The balance between extra- and intracellular fluids is maintained by their electrolyte composition and neuro-endocrine regulation. The role of potassium and sodium ions is especially important. They are selectively distributed on both sides of the cell membrane: potassium inside the cells, sodium in the extracellular fluid, creating an osmotic concentration gradient (“potassium-sodium pump”), providing tissue turgor.

In the regulation of water-salt metabolism, the leading role belongs to aldosterone and pituitary antidiuretic hormone (ADH). Aldosterone reduces the excretion of sodium as a result of increasing its reabsorption in the tubules of the kidneys, ADH controls the excretion of water by the kidneys, affecting its reabsorption.

Recognition of water metabolism disorders involves measuring the total amount of water in the body using the dilution method. It is based on the introduction into the body of indicators (antipyrine, heavy water), which are evenly distributed in the body. Knowing the amount of indicator entered TO and subsequently determining its concentration WITH, you can determine the total volume of liquid, which will be equal to K/S. The volume of circulating plasma is determined by diluting dyes (T-1824, Congo-mouth) that do not pass through the walls of the capillaries. Extracellular (extracellular) fluid is measured by the same dilution method using inulin, a radioisotope of 82 Br, which does not penetrate cells. The volume of interstitial fluid is determined by subtracting the volume of plasma from the volume of extracellular water, and intracellular fluid is determined by subtracting the amount of extracellular fluid from the total volume of water.

Important data on the disturbance of water balance in the body is obtained by studying the hydrophilicity of tissues (McClure and Aldrich test). An isotonic sodium chloride solution is injected into the skin until an infiltrate the size of a pea appears and its resorption is monitored. The more water the body loses, the faster the infiltrate disappears. In calves with dyspepsia, the blister resolves after 1.5-8 minutes (in healthy ones - after 20-25 minutes), in horses with mechanical intestinal obstruction - after 15-30 minutes (normally - after 3-5 hours).

Disturbances of water and electrolyte metabolism manifest themselves in various clinical forms. The most important are dehydration, water retention, hypo- and hypernatremia, hypo- and hyperkalemia.

Dehydration(exicosis, hypohydria, dehydration, negative water balance) with a simultaneous decrease in the osmotic pressure of the extracellular fluid (hypoosmolar dehydration) is observed with the loss of a large amount of fluid containing electrolytes (with vomiting, extensive burns), intestinal obstruction, swallowing disorders, diarrhea, hyperhidrosis, polyuria . Hyperosmolar dehydration is noted when a decrease in water occurs with a slight loss of electrolytes, and the lost fluid is not compensated for by drinking. The predominance of water loss over the release of electrolytes leads to an increase in the osmotic concentration of extracellular fluid and the release of water from cells into the intercellular space. This form of exicosis often develops in young animals with hyperventilation and diarrhea.

Dehydration syndrome manifested by general weakness, anorexia, thirst, dry mucous membranes and skin. Swallowing is difficult due to a lack of saliva. Oliguria develops, urine has a high relative density. Muscle turgor is reduced, enophthalmia occurs, and skin elasticity is reduced. Negative water balance, blood thickening, and loss of body weight are detected. Losing 10% of water in the body leads to serious consequences, and 20% leads to death.

Hyperhydria(water retention, edema, hyperhydration) occurs with a simultaneous decrease or increase in the osmotic pressure of the fluid (hypo- and hyperosmolar hyperhydration). Hypoosmolar overhydration recorded when large quantities of salt-free solutions are irrationally introduced into the animal’s body (orally or parenterally), especially after injuries, surgery, or when there is a decrease in water excretion by the kidneys. Hyperosmolar overhydration found when hypertonic solutions are excessively introduced into the body in volumes exceeding the ability to quickly remove them, in diseases of the heart, kidneys, and liver, leading to edema.

Overhydration syndrome(edematous) is characterized by lethargy, the appearance of doughy edema, and sometimes hydrops of the serous cavities develops. Body weight increases. Diuresis increases, urine has low relative density.

The content of sodium and potassium in feed, blood and plasma, tissues and body fluids is determined using a flame photometer, chemical methods or using radioactive isotopes 24 Na and 42 K. Whole blood of cattle contains sodium 260-280 mg/100 ml (113. 1-121.8 mmol/l), in plasma (serum) -320-340 mg/100 ml (139.2-147.9 mmol/l); potassium - in erythrocytes - 430-585 mg/100 ml (110.1-149.8 mmol/l), in whole blood - 38-42 mg/100 ml (9.73-10.75 mmol/l) and plasma -16- 29 mg/100 ml (4.1-5.12 mmol/l).

Sodium- the main cation of extracellular fluid (more than 90%), performing the functions of maintaining osmotic balance and as a component of buffer systems. The size of the extracellular space depends on the concentration of sodium: with an excess of it, the space increases, with a deficiency, it decreases.

Hyponatremia can be relative with an abundant intake of water in the body and absolute with sodium loss through sweat, diarrhea, vomiting, burns, nutritional dystrophy, or lack of sodium in the diet.

Hypernatremia develops due to loss of water or excess sodium chloride in the feed, with nephrosis, nephritis, wrinkled kidney, water starvation, diabetes insipidus, hypersecretion of aldosterone.

Hyponatremia syndrome manifested by vomiting, general weakness, decrease in body weight and water content in the body, decrease and perversion of appetite, drop in arterial blood pressure, acidosis and decrease in plasma sodium levels.

For hypernatremia syndrome they observe drooling, thirst, vomiting, increased body temperature, hyperemia of the mucous membranes, increased breathing and pulse, agitation, convulsions; the sodium content in the blood increases.

Potassium participates in maintaining intracellular osmotic pressure, acid-base balance, and neuromuscular excitability. 98.5% of potassium is found inside cells and only 1.5% is in extracellular fluid.

Hypokalemia occurs due to potassium deficiency in feed, with vomiting, diarrhea, edema, ascites, hypersecretion of aldosterone, and the use of saluretics.

Hyperkalemia develops when there is an excess intake of potassium from food or a decrease in its excretion. Increased potassium content is noted with hemolysis of red blood cells and increased tissue breakdown.

Hypokalemia syndrome characterized by anorexia, vomiting, atony of the stomach and intestines, muscle weakness; record cardiac weakness, paroxysmal tachycardia, tooth flattening T on ECG, weight loss. The level of potassium in the blood is reduced.

For hyperkalemia myocardial function is impaired (deafness of tones, extrasystole, bradycardia, decreased blood pressure, intraventricular block with ventricular fibrillation, wave T tall and sharp, complex QRS expanded, tooth R reduced or disappears).

Hyperpotassium toxicity syndrome accompanied by general weakness, oliguria, decreased neuromuscular excitability and cardiac decompensation.

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.

IN SURGICAL PATIENTSAND PRINCIPLES OF INFUSION THERAPY

Acute disturbances of water and electrolyte balance are one of the most common complications of surgical pathology - peritonitis, intestinal obstruction, pancreatitis, trauma, shock, diseases accompanied by fever, vomiting and diarrhea.

9.1. The main causes of water and electrolyte imbalances

The main causes of violations include:

external losses of fluid and electrolytes and their pathological redistribution between the main fluid environments due to pathological activation of natural processes in the body - with polyuria, diarrhea, excessive sweating, with profuse vomiting, through various drainages and fistulas or from the surface of wounds and burns;

internal movement of fluids during swelling of injured and infected tissues (fractures, crush syndrome); accumulation of fluid in the pleural (pleurisy) and abdominal (peritonitis) cavities;

changes in the osmolarity of fluids and the movement of excess water into or out of the cell.

Movement and accumulation of fluid in the gastrointestinal tract, reaching several liters (with intestinal obstruction, intestinal infarction, as well as with severe postoperative paresis) corresponds in severity to the pathological process external losses fluids, since in both cases large volumes of fluid with a high content of electrolytes and protein are lost. No less significant external losses of fluid identical to plasma from the surface of wounds and burns (into the pelvic cavity), as well as during extensive gynecological, proctological and thoracic operations (into the pleural cavity).

Internal and external fluid loss determine the clinical picture of fluid deficiency and water-electrolyte imbalance: hemoconcentration, plasma deficiency, protein loss and general dehydration. In all cases, these disorders require targeted correction of water and electrolyte balance. Being unrecognized and unresolved, they worsen the results of treatment of patients.

The entire water supply of the body is located in two spaces - intracellular (30-40% of body weight) and extracellular (20-27% of body weight).

Extracellular volume distributed between interstitial water (water of ligaments, cartilage, bones, connective tissue, lymph, plasma) and water that does not actively participate in metabolic processes (cerebrospinal, intra-articular fluid, gastrointestinal contents).

Intracellular sector contains water in three forms (constitutional, protoplasm and colloidal micelles) and electrolytes dissolved in it. Cellular water is distributed unevenly in various tissues, and the more hydrophilic they are, the more vulnerable they are to disturbances in water metabolism. Some of the cellular water is formed as a result of metabolic processes.

The daily volume of metabolic water during the “burning” of 100 g of proteins, fats and carbohydrates is 200-300 ml.

The volume of extracellular fluid can increase with injury, fasting, sepsis, severe infectious diseases, i.e., with those conditions that are accompanied by significant loss of muscle mass. An increase in the volume of extracellular fluid occurs during edema (cardiac, protein-free, inflammatory, renal, etc.).

The volume of extracellular fluid decreases with all forms of dehydration, especially with loss of salts. Significant disturbances are observed in critical conditions in surgical patients - peritonitis, pancreatitis, hemorrhagic shock, intestinal obstruction, blood loss, severe trauma. The ultimate goal of regulating water and electrolyte balance in such patients is to maintain and normalize vascular and interstitial volumes, their electrolyte and protein composition.

Maintenance and normalization of the volume and composition of extracellular fluid are the basis for the regulation of arterial and central venous pressure, cardiac output, organ blood flow, microcirculation and biochemical homeostasis.

Maintaining the body's water balance normally occurs through adequate water intake in accordance with its losses; The daily “turnover” is about 6% of the body’s total water. An adult consumes approximately 2500 ml of water per day, of which 300 ml of water is formed as a result of metabolic processes. Water loss is about 2500 ml/day, of which 1500 ml is excreted in urine, 800 ml evaporates (400 ml through the respiratory tract and 400 ml through the skin), 100 ml is excreted in sweat and 100 ml in feces. When carrying out corrective infusion-transfusion therapy and parenteral nutrition, the mechanisms that regulate the flow and consumption of fluid and thirst are shunted. Therefore, careful monitoring of clinical and laboratory data, body weight and daily urine output is required to restore and maintain normal hydration status. It should be noted that physiological fluctuations in water loss can be quite significant. As body temperature rises, the amount of endogenous water increases and water loss through the skin during respiration increases. Breathing disorders, especially hyperventilation at low air humidity, increase the body's need for water by 500-1000 ml. Loss of fluid from extensive wound surfaces or during long-term surgical interventions on the abdominal and thoracic cavities for more than 3 hours increases the need for water to 2500 ml/day.

If the supply of water prevails over its release, the water balance is calculated positive; against the background of functional disorders of the excretory organs, it is accompanied by the development of edema.

When water release predominates over intake, the balance is calculated negative- in this case, a feeling of thirst serves as a signal of dehydration.

Untimely correction of dehydration can lead to collapse or dehydration shock.

The main organ regulating water and electrolyte balance is the kidneys. The volume of urine excreted is determined by the amount of substances that need to be removed from the body and the ability of the kidneys to concentrate urine.

From 300 to 1500 mmol of metabolic end products are excreted in the urine per day. With a lack of water and electrolytes, oliguria and anuria resolve

viewed as a physiological response associated with stimulation of ADH and aldosterone. Correction of water and electrolyte losses leads to restoration of diuresis.

Normally, the regulation of water balance is carried out by activating or inhibiting the osmoreceptors of the hypothalamus, which respond to changes in plasma osmolarity, the feeling of thirst arises or is suppressed, and the secretion of antidiuretic hormone (ADH) of the pituitary gland changes accordingly. ADH increases water reabsorption in the distal tubules and collecting ducts of the kidneys and reduces urine output. On the contrary, with a decrease in ADH secretion, urination increases and urine osmolarity decreases. The formation of ADH naturally increases with a decrease in fluid volumes in the interstitial and intravascular sectors. With an increase in blood volume, the secretion of ADH decreases.

In pathological conditions, factors such as hypovolemia, pain, traumatic tissue damage, vomiting, and medications that affect the central mechanisms of nervous regulation of water and electrolyte balance are of additional importance.

There is a close relationship between the amount of fluid in various sectors of the body, the state of peripheral circulation, capillary permeability and the ratio of colloid-osmotic and hydrostatic pressures.

Normally, the exchange of fluid between the vascular bed and the interstitial space is strictly balanced. In pathological processes associated primarily with the loss of protein circulating in the plasma (acute blood loss, liver failure), the plasma COD decreases, as a result of which excess fluid from the microcirculatory system passes into the interstitium. The blood thickens and its rheological properties are disrupted.

9.2. Electrolyte metabolism

The state of water metabolism in normal and pathological conditions is closely interconnected with the exchange of electrolytes - Na +, K +, Ca 2+, Mg 2+, SG, HC0 3, H 2 P0 4 ~, SOf, as well as proteins and organic acids.

The concentration of electrolytes in the fluid spaces of the body is not the same; plasma and interstitial fluid differ significantly only in protein content.

The content of electrolytes in the extra- and intracellular fluid spaces is not the same: the extracellular contains mainly Na +, SG, HCO^; in the intracellular - K +, Mg + and H 2 P0 4; the concentration of S0 4 2 and proteins is also high. Differences in the concentrations of certain electrolytes form a resting bioelectric potential, which imparts excitability to nerve, muscle and sector cells.

Preservation of electrochemical potential cellular and extracellularspace is ensured by the operation of the Na + -, K + -ATPase pump, thanks to which Na + is constantly “pumped out” of the cell, and K + - is “driven” into it against their concentration gradients.

When this pump is disrupted due to oxygen deficiency or as a result of metabolic disorders, the cellular space becomes available for sodium and chlorine. The accompanying increase in osmotic pressure in the cell increases the movement of water in it, causing swelling,

and subsequently a violation of the integrity of the membrane, up to lysis. Thus, the dominant cation in the intercellular space is sodium, and in the cell - potassium.

9.2.1. Sodium metabolism

Sodium - main extracellular cation; the most important cation of the interstitial space is the main osmotically active substance in the plasma; participates in the generation of action potentials, affects the volume of extracellular and intracellular spaces.

As Na + concentration decreases, osmotic pressure decreases with a simultaneous decrease in the volume of the interstitial space. An increase in sodium concentration causes the opposite process. Sodium deficiency cannot be compensated by any other cation. The daily sodium requirement of an adult is 5-10 g.

Sodium is excreted from the body mainly by the kidneys; a small part comes from sweat. Its level in the blood increases with prolonged treatment with corticosteroids, prolonged mechanical ventilation in hyperventilation mode, diabetes insipidus, and hyperaldosteronism; decreases due to long-term use of diuretics, against the background of prolonged heparin therapy, in the presence of chronic heart failure, hyperglycemia, and cirrhosis of the liver. The normal sodium content in urine is 60 mmol/l. Surgical aggression associated with activation of antidiuretic mechanisms leads to sodium retention at the kidney level, so its content in urine may decrease.

Hypernatremia(plasma sodium more than 147 mmol/l) occurs with an increased sodium content in the interstitial space, as a result of dehydration due to water depletion, salt overload of the body, and diabetes insipidus. Hypernatremia is accompanied by a redistribution of fluid from the intracellular to the extracellular sector, which causes cell dehydration. In clinical practice, this condition occurs due to increased sweating, intravenous infusion of hypertonic sodium chloride solution, and also due to the development of acute renal failure.

Hyponatremia(plasma sodium less than 136 mmol/l) develops with excessive secretion of ADH in response to a pain factor, with pathological fluid losses through the gastrointestinal tract, excessive intravenous administration of salt-free solutions or glucose solutions, excessive water intake against the background of limited food intake; accompanied by hyperhydration of cells with a simultaneous decrease in BCC.

Sodium deficiency is determined by the formula:

For deficit (mmol) = (Na HOpMa - actual number) body weight (kg) 0.2.

9.2.2. Potassium metabolism

Potassium - main intracellular cation. The daily requirement for potassium is 2.3-3.1 g. Potassium (together with sodium) takes an active part in all metabolic processes of the body. Potassium, like sodium, plays a leading role in the formation of membrane potentials; it affects pH and glucose utilization and is necessary for protein synthesis.

In the postoperative period, in critical conditions, potassium losses may exceed its intake; they are also typical for long-term fasting, accompanied by loss of cell mass of the body - the main “depot” of potassium. Hepatic glycogen metabolism plays a certain role in increasing potassium losses. In seriously ill patients (without appropriate compensation), up to 300 mmol of potassium moves from the cellular space to the extracellular space in 1 week. In the early post-traumatic period, potassium leaves the cell along with metabolic nitrogen, the excess of which is formed as a result of cellular protein catabolism (on average, 1 g of nitrogen “carries away” 5-6 meq of potassium).

Imonk.temia(plasma potassium less than 3.8 mmol/l) can develop with an excess of sodium, against the background of metabolic alkalosis, with hypoxia, severe protein catabolism, diarrhea, prolonged vomiting, etc. With intracellular potassium deficiency, Na + and H + enter the cell intensively, which causes intracellular acidosis and hyperhydration against the background of extracellular metabolic alkalosis. Clinically, this condition is manifested by arrhythmia, arterial hypotension, decreased skeletal muscle tone, intestinal paresis, and mental disorders. Characteristic changes appear on the ECG: tachycardia, narrowing of the complex QRS, flattening and inversion of the tooth T, increase in tooth amplitude U. Treatment of hypokalemia begins by eliminating the etiological factor and compensating for potassium deficiency, using the formula:

Potassium deficiency (mmol/l) = K + patient plasma, mmol/l 0.2 body weight, kg.

Rapid administration of large amounts of potassium preparations can cause cardiac complications, including cardiac arrest, so the total daily dose should not exceed 3 mmol/kg/day, and the infusion rate should not exceed 10 mmol/h.

Potassium preparations used should be diluted (up to 40 mmol per 1 liter of injected solution); it is optimal to administer them in the form of a polarizing mixture (glucose + potassium + insulin). Treatment with potassium preparations is carried out under daily laboratory supervision.

Hyperkalemia(plasma potassium more than 5.2 mmol/l) most often occurs when there is a violation of the excretion of potassium from the body (acute renal failure) or when it is massively released from damaged cells due to extensive trauma, hemolysis of red blood cells, burns, positional compression syndrome, etc. In addition, , hyperkalemia is characteristic of hyperthermia, convulsive syndrome and accompanies the use of a number of drugs - heparin, aminocaproic acid, etc.

Diagnostics hyperkalemia is based on the presence of etiological factors (trauma, acute renal failure), the appearance of characteristic changes in cardiac activity: sinus bradycardia (up to cardiac arrest) in combination with ventricular extrasystole, pronounced slowing of intraventricular and atrioventricular conduction and characteristic laboratory data (plasma potassium more than 5. 5 mmol/l). A high, pointed wave is recorded on the ECG T, expansion of the complex QRS, reduction in tooth amplitude R.

Treatment hyperkalemia begins with eliminating the etiological factor and correcting acidosis. Calcium supplements are prescribed; To transfer excess plasma potassium into the cell, a glucose solution (10-15%) with insulin is injected intravenously (1 unit for every 3-4 g of glucose). If these methods do not produce the desired effect, hemodialysis is indicated.

9.2.3. Calcium metabolism

Calcium is approximately 2 % body weight, 99% of which are in a bound state in the bones and under normal conditions do not take part in electrolyte metabolism. The ionized form of calcium is actively involved in the neuromuscular transmission of excitation, blood coagulation processes, the work of the heart muscle, the formation of the electrical potential of cell membranes and the production of a number of enzymes. The daily requirement is 700-800 mg. Calcium enters the body with food, is excreted through the gastrointestinal tract and in the urine. Calcium metabolism is closely related to phosphorus metabolism, plasma protein levels and blood pH.

Hypocalcemia(plasma calcium less than 2.1 mmol/l) develops with hypoalbuminemia, pancreatitis, transfusion of large amounts of citrated blood, long-standing biliary fistulas, vitamin D deficiency, malabsorption in the small intestine, after highly traumatic operations. Clinically manifested by increased neuromuscular excitability, paresthesia, paroxysmal tachycardia, tetany. Correction of hypocalcemia is carried out after laboratory determination of its level in the blood plasma by intravenous administration of drugs containing ionized calcium (gluconate, lactate, chloride or calcium carbonate). The effectiveness of corrective therapy for hypocalcemia depends on the normalization of albumin levels.

Hypercalcemia(plasma calcium more than 2.6 mmol/l) occurs in all processes accompanied by increased bone destruction (tumors, osteomyelitis), diseases of the parathyroid glands (adenoma or parathyroiditis), excessive administration of calcium supplements after citrated blood transfusion, etc. Clinical condition manifested by increased fatigue, lethargy, and muscle weakness. As hypercalcemia increases, symptoms of gastrointestinal atony appear: nausea, vomiting, constipation, flatulence. A characteristic shortening of the interval appears on the ECG (2-7; rhythm and conduction disturbances, sinus bradycardia, slowing of atrioventricular conduction are possible; the G wave may become negative, biphasic, reduced, rounded.

Treatment is to influence the pathogenetic factor. In case of severe hypercalcemia (more than 3.75 mmol/l), targeted correction is required - 2 g of disodium salt of ethylenediaminetetraacetic acid (EDTA), diluted in 500 ml of 5% glucose solution, is administered slowly intravenously, dropwise 2-4 times a day, under control of calcium levels in blood plasma.

9.2.4. Magnesium metabolism

Magnesium is an intracellular cation; its concentration in plasma is 2.15 times less than inside erythrocytes. The microelement reduces neuromuscular excitability and myocardial contractility and causes depression of the central nervous system. Magnesium plays a huge role in the absorption of oxygen by cells, energy production, etc. It enters the body with food and is excreted through the gastrointestinal tract and urine.

Hypomagnesemia(plasma magnesium less than 0.8 mmol/l) is observed in liver cirrhosis, chronic alcoholism, acute pancreatitis, polyuric stage of acute renal failure, intestinal fistulas, unbalanced infusion therapy. Clinically, hypomagnesemia manifests itself as increased nervousness

muscle excitability, hyperreflexia, convulsive contractions of various muscle groups; Spastic pain in the gastrointestinal tract, vomiting, and diarrhea may occur. Treatment consists of a targeted impact on the etiological factor and the administration of magnesium salts under laboratory control.

Hypermagnesemia(plasma magnesium more than 1.2 mmol/l) develops with ketoacidosis, increased catabolism, acute renal failure. Clinically manifested by drowsiness and lethargy, hypotension and bradycardia, decreased breathing with the appearance of signs of hypoventilation. Treatment- targeted impact on the etiological factor and the appointment of a magnesium antagonist - calcium salts.

9.2.5. Chlorine exchange

Chlorine - main anion of the extracellular space; is in equivalent proportions with sodium. It enters the body in the form of sodium chloride, which dissociates Na + and C1 in the stomach." When it combines with hydrogen, chlorine forms hydrochloric acid.

Hypochloremia(plasma chlorine less than 95 mmol/l) develops with prolonged vomiting, peritonitis, pyloric stenosis, high intestinal obstruction, increased sweating. The development of hypochloremia is accompanied by an increase in the bicarbonate buffer and the appearance of alkalosis. Clinically manifested by dehydration, respiratory and cardiac dysfunction. A convulsive or comatose state may occur with a fatal outcome. Treatment consists of a targeted impact on the pathogenetic factor and carrying out infusion therapy with chlorides (primarily sodium chloride preparations) under laboratory control.

Hyperchloremia(plasma chlorine more than PO mmol/l) develops with general dehydration, impaired removal of fluid from the interstitial space (for example, acute renal failure), increased transition of fluid from the vascular bed to the interstitium (with hypoproteinemia), and the introduction of large volumes of liquids containing excess amounts of chlorine. The development of hyperchloremia is accompanied by a decrease in the buffer capacity of the blood and the appearance of metabolic acidosis. Clinically, this is manifested by the development of edema. The basic principle treatment- impact on the pathogenetic factor in combination with syndromic therapy.

9.3. Main types of water-electrolyte metabolism disorders

▲ Isotonic dehydration(plasma sodium within normal limits: 135-145 mmol/l) occurs due to loss of fluid in the interstitial space. Since the electrolyte composition of the interstitial fluid is close to blood plasma, a uniform loss of fluid and sodium occurs. Most often, isotonic dehydration develops with prolonged vomiting and diarrhea, acute and chronic gastrointestinal diseases, intestinal obstruction, peritonitis, pancreatitis, extensive burns, polyuria, uncontrolled use of diuretics, and polytrauma. Dehydration is accompanied by a loss of electrolytes without a significant change in plasma osmolarity, therefore, a significant redistribution of water between sectors does not occur, but hypovolemia is formed. Clinically

disturbances in central hemodynamics are noted. Skin turgor is reduced, the tongue is dry, oliguria up to anuria. Treatment pathogenetic; replacement therapy with isotonic sodium chloride solution (35-70 ml/kg/day). Infusion therapy should be carried out under the control of central venous pressure and hourly diuresis. If correction of hypotonic dehydration is carried out against the background of metabolic acidosis, sodium is administered in the form of bicarbonate; in metabolic alkalosis - in the form of chloride.

▲ Hypotonic dehydration(plasma sodium less than 130 mmol/l) develops in cases where sodium losses exceed water losses. Occurs with massive losses of fluids containing large amounts of electrolytes - repeated vomiting, profuse diarrhea, profuse sweating, polyuria. A decrease in sodium content in plasma is accompanied by a decrease in its osmolarity, as a result of which water from the plasma begins to be redistributed into cells, causing their swelling (intracellular hyperhydration) and creating water deficiency in the interstitial space.

Clinically this condition is manifested by decreased turgor of the skin and eyeballs, impaired hemodynamics and volume, azotemia, impaired renal and brain function, and hemoconcentration. Treatment consists of a targeted impact on the pathogenetic factor and active rehydration with solutions containing sodium, potassium, magnesium (ace-salt). For hyperkalemia, disol is prescribed.

▲ Hypertensive dehydration(plasma sodium more than 150 mmol/l) occurs due to excess water loss over sodium loss. Occurs during the polyuric stage of acute renal failure, prolonged forced diuresis without timely replenishment of water deficiency, fever, and insufficient administration of water during parenteral nutrition. The excess of water loss over sodium causes an increase in plasma osmolarity, as a result of which intracellular fluid begins to pass into the vascular bed. Intracellular dehydration is formed (cellular dehydration, exicosis).

Clinical symptoms- thirst, weakness, apathy, drowsiness, and in severe cases - psychosis, hallucinations, dry tongue, increased body temperature, oliguria with high relative density of urine, azotemia. Dehydration of brain cells causes the appearance of nonspecific neurological symptoms: psychomotor agitation, confusion, convulsions, development of a coma.

Treatment consists of a targeted impact on the pathogenetic factor and the elimination of intracellular dehydration by prescribing infusions of a glucose solution with insulin and potassium. The administration of hypertonic solutions of salts, glucose, albumin, and diuretics is contraindicated. Monitoring of plasma sodium levels and osmolarity is necessary.

▲ Isotonic hyperhydration(plasma sodium within the normal range of 135-145 mmol/l) most often occurs against the background of diseases accompanied by edema syndrome (chronic heart failure, toxicosis of pregnancy), as a result of excessive administration of isotonic saline solutions. The occurrence of this syndrome is also possible against the background of liver cirrhosis and kidney diseases (nephrosis, glomerulonephritis). The main mechanism for the development of isotonic overhydration is excess water and salts with normal plasma osmolarity. Fluid retention occurs mainly in the interstitial space.

Clinically this form of hyperhydration is manifested by the appearance of arterial hypertension, rapid increase in body weight, development of edema syndrome, anasarca, and decrease in blood concentration parameters. Against the background of overhydration, there is a deficiency of free fluid.

Treatment consists in the use of diuretics aimed at reducing the volume of interstitial space. In addition, 10% albumin is administered intravenously to increase the oncotic pressure of the plasma, as a result of which the interstitial fluid begins to pass into the vascular bed. If this treatment does not give the desired effect, they resort to hemodialysis with ultrafiltration of blood.

Hyperhydration hypotonic(plasma sodium less than 130 mmol/l), or “water poisoning,” can occur with the simultaneous intake of very large quantities of water, with prolonged intravenous administration of salt-free solutions, edema due to chronic heart failure, cirrhosis of the liver, surge arrester, hyperproduction of ADH. The main mechanism is a decrease in plasma osmolarity and the transfer of fluid into the cells.

Clinical picture manifested by vomiting, frequent loose, watery stools, and polyuria. Signs of central nervous system damage are added: weakness, weakness, fatigue, sleep disturbance, delirium, impaired consciousness, convulsions, coma.

Treatment consists in removing excess water from the body as quickly as possible: diuretics are prescribed with simultaneous intravenous administration of sodium chloride and vitamins. A high-calorie diet is required. If necessary, hemodialysis with blood ultrafiltration is performed.

and Hyperhydration hypertensive(plasma sodium more 150 mmol/l) occurs when large quantities of hypertonic solutions are introduced into the body against the background of preserved excretory function of the kidneys or isotonic solutions - to patients with impaired excretory function of the kidneys. The condition is accompanied by an increase in the osmolarity of the fluid in the interstitial space, followed by dehydration of the cellular sector and increased release of potassium from it.

Clinical picture characterized by thirst, redness of the skin, increased body temperature, blood pressure and central venous pressure. As the process progresses, signs of central nervous system damage appear: mental disorders, convulsions, coma.

Treatment- infusion therapy with inclusion 5 % solution of glucose and albumin against the background of stimulation of diuresis with osmodiuretics and saluretics. According to indications - hemodialysis.

9.4. Acid-base state

Acid-base state(COS) is one of the most important components of the biochemical constancy of body fluids as the basis of normal metabolic processes, the activity of which depends on the chemical reaction of the electrolyte.

CBS is characterized by the concentration of hydrogen ions and is designated by the pH symbol. Acidic solutions have a pH from 1.0 to 7.0, basic solutions - from 7.0 to 14.0. Acidosis- a shift in pH to the acidic side occurs due to the accumulation of acids or a lack of bases. Alkalosis- a shift in pH to the alkaline side is caused by an excess of bases or a decrease in acid content. Constancy of pH is an indispensable condition of human life. pH is the final, overall reflection of the equilibrium of the concentration of hydrogen ions (H +) and the body's buffer systems. Maintaining the equilibrium of the CBS

carried out by two systems that prevent a shift in blood pH. These include buffer (physicochemical) and physiological systems for the regulation of CBS.

9.4.1. Physico-chemical buffer systems

There are four known physicochemical buffer systems of the body - bicarbonate, phosphate, blood protein buffer system, hemoglobin.

Bicarbonate system making up 10% of the total buffer capacity of the blood, it is the ratio of bicarbonates (HC0 3) and carbon dioxide (H 2 CO 3). Normally it is 20:1. The end product of the interaction between bicarbonates and acid is carbon dioxide (CO 2), which is exhaled. The bicarbonate system is the fastest acting and works both in plasma and in extracellular fluid.

Phosphate system takes up little space in buffer tanks (1%), acts more slowly, and the final product - potassium sulfate - is excreted by the kidneys.

Plasma proteins Depending on the pH level, they can act as both acids and bases.

Hemoglobin buffer system occupies a major role in maintaining the acid-base state (about 70% of the buffer capacity). Hemoglobin in erythrocytes binds 20% of the incoming blood, carbon dioxide (C0 2), as well as hydrogen ions formed due to the dissociation of carbon dioxide (H 2 C0 3).

The bicarbonate buffer is predominantly present in the blood and in all parts of the extracellular fluid; in plasma - bicarbonate, phosphate and protein buffers; in erythrocytes - hydrocarbonate, protein, phosphate, hemoglobin; in urine - phosphate.

9.4.2. Physiological buffer systems

Lungs regulate the content of CO 2, which is a decomposition product of carbonic acid. The accumulation of CO 2 leads to hyperventilation and shortness of breath, and thus excess carbon dioxide is removed. If there is an excess of bases, the reverse process occurs - pulmonary ventilation decreases, and bradypnea occurs. Along with CO2, blood pH and oxygen concentration are strong irritants of the respiratory center. Shifts in pH and changes in oxygen concentration lead to increased pulmonary ventilation. Potassium salts act in a similar way, but with a rapid increase in the concentration of K + in the blood plasma, the activity of chemoreceptors is suppressed and pulmonary ventilation is reduced. The respiratory regulation of the CBS is a rapid response system.

Kidneys support CBS in several ways. Under the influence of the enzyme carbonic anhydrase, which is contained in large quantities in the kidney tissue, C0 2 and H 2 0 combine to form carbonic acid. Carbonic acid dissociates into bicarbonate (HC0 3 ~) and H +, which combines with the phosphate buffer and is excreted in the urine. Bicarbonates are reabsorbed in the tubules. However, when bases are in excess, reabsorption is reduced, resulting in increased urinary excretion of bases and decreased alkalosis. Each millimole of H + excreted in the form of titratable acids or ammonium ions adds 1 mmol to the blood plasma

HC0 3 . Thus, H + excretion is closely related to the synthesis of HC0 3. Renal regulation of CBS is slow and requires many hours or even days for full compensation.

Liver regulates CBS by metabolizing under-oxidized metabolic products coming from the gastrointestinal tract, forming urea from nitrogenous wastes and removing acid radicals with bile.

Gastrointestinal tract occupies an important place in maintaining the constancy of CBS due to the high intensity of the processes of intake and absorption of liquids, food and electrolytes. Violation of any part of digestion causes disruption of the CBS.

Chemical and physiological buffer systems are powerful and effective mechanisms for compensating for CBS. In this regard, even the slightest changes in CBS indicate severe metabolic disorders and dictate the need for timely and targeted corrective therapy. General directions for normalizing CBS include eliminating the etiological factor (pathology of the respiratory and cardiovascular systems, abdominal organs, etc.), normalizing hemodynamics - correcting hypovolemia, restoring microcirculation, improving the rheological properties of blood, treating respiratory failure, up to transferring the patient to mechanical ventilation , correction of water-electrolyte and protein metabolism.

WWTP indicators determined by the Astrupa equilibration micromethod (with interpolation calculation of рС0 2) or by methods with direct oxidation of С0 2. Modern microanalyzers automatically determine all values ​​of CBS and partial voltage of blood gases. The main indicators of the WWTP are presented in table. 9.1.

Table 9.1.CBS indicators are normal

To assess the type of CBS violation in normal practical work, the indicators pH, PC0 2, P0 2, BE are used.

9.4.3. Types of acid-base imbalance

There are 4 main types of CBS disorders: metabolic acidosis and alkalosis; respiratory acidosis and alkalosis; Combinations of these are also possible.

A Metabolic acidosis- base deficiency, leading to a decrease in pH. Causes: acute renal failure, uncompensated diabetes (ketoacidosis), shock, heart failure (lactic acidosis), poisoning (salicylates, ethylene glycol, methyl alcohol), small intestinal (duodenal, pancreatic) fistulas, diarrhea, adrenal insufficiency. CBS indicators: pH 7.4-7.29, PaC0 2 40-28 Hg. Art., BE 0-9 mmol/l.

Clinical symptoms- nausea, vomiting, weakness, disturbances of consciousness, tachypnea. Clinically, moderate acidosis (BE up to -10 mmol/l) may be asymptomatic. When the pH decreases to 7.2 (state of subcompensation, then decompensation), shortness of breath increases. With a further decrease in pH, respiratory and heart failure increases, and hypoxic encephalopathy develops up to coma.

Treatment of metabolic acidosis:

Strengthening the bicarbonate buffer system - introducing a 4.2% sodium bicarbonate solution (contraindications- hypokalemia, metabolic alkalosis, hypernatremia) intravenously through a peripheral or central vein: undiluted, diluted with 5% glucose solution in a 1:1 ratio. The solution infusion rate is 200 ml per 30 minutes. The required amount of sodium bicarbonate can be calculated using the formula:

Amount of mmol sodium bicarbonate = BE body weight, kg 0.3.

Without laboratory control, use no more than 200 ml/day, dropwise, slowly. The solution should not be administered simultaneously with solutions containing calcium, magnesium and should not be mixed with phosphate-containing solutions. Transfusion of lactasol according to the mechanism of action is similar to the use of sodium bicarbonate.

A Metabolic alkalosis- a state of deficiency of H + ions in the blood in combination with an excess of bases. Metabolic alkalosis is difficult to treat, as it is the result of both external losses of electrolytes and disorders of cellular and extracellular ionic relations. Such disorders are typical for massive blood loss, refractory shock, sepsis, severe losses of water and electrolytes during intestinal obstruction, peritonitis, pancreatic necrosis, and long-term intestinal fistulas. Quite often, it is metabolic alkalosis, as the final phase of metabolic disorders incompatible with life in this category of patients, that becomes the direct cause of death.

Principles of correction of metabolic alkalosis. Metabolic alkalosis is easier to prevent than to treat. Preventive measures include adequate administration of potassium during blood transfusion therapy and replenishment of cellular potassium deficiency, timely and complete correction of volemic and hemodynamic disorders. When treating established metabolic alkalosis, it is of paramount importance

elimination of the main pathological factor of this condition. Purposeful normalization of all types of exchange is carried out. Relief of alkalosis is achieved by intravenous administration of protein preparations, glucose solutions in combination with potassium chloride, and large amounts of vitamins. An isotonic sodium chloride solution is used to reduce the osmolarity of extracellular fluid and eliminate cellular dehydration.

▲ Respiratory (breathing) acidosis characterized by an increase in the blood concentration of H + ions (pH< 7,38), рС0 2 (>40 mmHg Art.), BE (= 3.5+12 mmol/l).

The causes of respiratory acidosis can be hypoventilation as a result of obstructive forms of pulmonary emphysema, bronchial asthma, impaired ventilation in weakened patients, extensive atelectasis, pneumonia, acute pulmonary injury syndrome.

The main compensation for respiratory acidosis is carried out by the kidneys through forced excretion of H + and SG, increasing the reabsorption of HC0 3.

IN clinical picture respiratory acidosis is dominated by symptoms of intracranial hypertension, which arise due to cerebral vasodilation caused by excess CO 2 . Progressive respiratory acidosis leads to cerebral edema, the severity of which corresponds to the degree of hypercapnia. Stupor often develops and progresses to coma. The first signs of hypercapnia and increasing hypoxia are the patient’s anxiety, motor agitation, arterial hypertension, tachycardia with subsequent transition to hypotension and tachyarrhythmia.

Treatment of respiratory acidosis primarily consists of improving alveolar ventilation, eliminating atelectasis, pneumo- or hydrothorax, sanitation of the tracheobronchial tree and transferring the patient to mechanical ventilation. Treatment must be carried out urgently, before hypoxia develops as a result of hypoventilation.

and Respiratory (breathing) alkalosis characterized by a decrease in pCO 2 level below 38 mm Hg. Art. and a rise in pH above 7.45-7.50 as a result of increased ventilation of the lungs both in frequency and depth (alveolar hyperventilation).

The leading pathogenetic element of respiratory alkalosis is a decrease in volumetric cerebral blood flow as a result of increased cerebral vascular tone, which is a consequence of CO2 deficiency in the blood. In the initial stages, the patient may experience paresthesia of the skin of the extremities and around the mouth, muscle spasms in the extremities, mild or severe drowsiness, headache, and sometimes deeper disturbances of consciousness, even coma.

Prevention and treatment respiratory alkalosis are primarily aimed at normalizing external respiration and influencing the pathogenetic factor that caused hyperventilation and hypocapnia. Indications for transferring a patient to mechanical ventilation are depression or absence of spontaneous breathing, as well as shortness of breath and hyperventilation.

9.5. Infusion therapy for fluid and electrolyte disturbances and acid-base status

Infusion therapy is one of the main methods in the treatment and prevention of dysfunctions of vital organs and systems in surgical patients. Efficiency of infusion

therapy depends on the validity of its program, the characteristics of infusion media, pharmacological properties and pharmacokinetics of the drug.

For diagnostics volemic disorders and construction infusion therapy programs in the pre- and postoperative period, skin turgor, moisture of the mucous membranes, pulse filling in the peripheral artery, heart rate and blood pressure are important. During surgery, peripheral pulse filling, hourly diuresis, and blood pressure dynamics are most often assessed.

Manifestations of hypervolemia are tachycardia, shortness of breath, moist rales in the lungs, cyanosis, foamy sputum. The degree of volemic disorders is reflected by laboratory data - hematocrit, arterial blood pH, relative density and osmolarity of urine, concentration of sodium and chlorine in urine, sodium in plasma.

To laboratory signs dehydration include an increase in hematocrit, progressive metabolic acidosis, a relative density of urine more than 1010, a decrease in the concentration of Na + in the urine less than 20 mEq/L, and urine hyperosmolarity. There are no laboratory signs characteristic of hypervolemia. Hypervolemia can be diagnosed based on chest x-ray data - increased vascular pulmonary pattern, interstitial and alveolar pulmonary edema. CVP is assessed according to the specific clinical situation. The most revealing is the volumetric load test. A slight increase (1-2 mm Hg) in CVP after a rapid infusion of crystalloid solution (250-300 ml) indicates hypovolemia and the need to increase the volume of infusion therapy. And vice versa, if after the test the increase in central venous pressure exceeds 5 mm Hg. Art., it is necessary to reduce the rate of infusion therapy and limit its volume. Infusion therapy involves intravenous administration of colloid and crystalloid solutions.

A Crystalloid solutions - aqueous solutions of low molecular weight ions (salts) quickly penetrate the vascular wall and are distributed in the extracellular space. The choice of solution depends on the nature of the fluid loss that needs to be replenished. Loss of water is replaced with hypotonic solutions, which are called maintenance solutions. The deficiency of water and electrolytes is replenished with isotonic electrolyte solutions, which are called replacement solutions.

▲ Colloidal solutions based on gelatin, dextran, hydroxyethyl starch and polyethylene glycol, they maintain the colloid-osmotic pressure of the plasma and circulate in the vascular bed, providing a volemic, hemodynamic and rheological effect.

In the perioperative period, with the help of infusion therapy, physiological needs for fluid are met (maintenance therapy), concomitant fluid deficiency, and losses through the surgical wound. The choice of infusion solution depends on the composition and nature of the fluid being lost - sweat, the contents of the gastrointestinal tract. Intraoperative loss of water and electrolytes is caused by evaporation from the surface of the surgical wound during extensive surgical interventions and depends on the area of ​​the wound surface and the duration of the operation. Accordingly, intraoperative fluid therapy includes replenishing basic physiological fluid needs, eliminating preoperative deficits and operative losses.

Table 9.2. Electrolyte content in the gastrointestinal tract

Water requirement determined based on an accurate assessment of the resulting fluid deficiency, taking into account renal and extrarenal losses.

For this purpose, the volume of daily diuresis is summed up: V, - the proper value is 1 ml/kg/h; V 2 - losses through vomiting, stool and gastrointestinal contents; V 3 - drainage discharge; P - losses by perspiration through the skin and lungs (10-15 ml/kg/day), taking into account the constant T - losses during fever (with an increase in body temperature by 1 ° C above 37 ° C, losses are 500 ml per day). Thus, the total daily water deficit is calculated using the formula:

E = V, + V 2 + V 3 + P + T (ml).

To prevent hypo- or overhydration, it is necessary to control the amount of fluid in the body, in particular, that located in the extracellular space:

OVZh = body weight, kg 0.2, conversion factor Hematocrit - Hematocrit

Deficiency = true proper body weight, kg Hematocrit proper 5

Calculation of essential electrolyte deficiency(K + , Na +) are produced taking into account the volumes of their losses in urine, the contents of the gastrointestinal tract (GIT) and drainage media; determination of concentration indicators - according to generally accepted biochemical methods. If it is impossible to determine potassium, sodium, chlorine in gastric contents, losses can be assessed primarily taking into account fluctuations in the concentrations of indicators within the following limits: Na + 75-90 mmol/l; K + 15-25 mmol/l, SG up to 130 mmol/l, total nitrogen 3-5.5 g/l.

Thus, the total loss of electrolytes per day is:

E = V, C, + V 2 C 2 + V 3 C 3 g,

where V] is daily diuresis; V 2 - volume of gastrointestinal tract discharge during vomiting, with stool, by tube, as well as fistula losses; V 3 - discharge through drainage from the abdominal cavity; C, C 2, C 3 - concentration indicators in these environments, respectively. When calculating, you can refer to the data in table. 9.2.

When converting the loss value from mmol/l (SI system) to grams, the following conversions must be performed:

K +, g = mmol/l 0.0391.

Na +, g = mmol/l 0.0223.

9.5.1. Characteristics of crystalloid solutions

Agents that regulate water-electrolyte and acid-base homeostasis include electrolyte solutions and osmodiuretics. Electrolyte solutions used to correct disorders of water metabolism, electrolyte metabolism, water-electrolyte metabolism, acid-base state (metabolic acidosis), water-electrolyte metabolism and acid-base state (metabolic acidosis). The composition of electrolyte solutions determines their properties - osmolarity, isotonicity, ionicity, reserve alkalinity. In relation to the osmolarity of electrolyte solutions to blood, they exhibit an iso-, hypo-, or hyperosmolar effect.

Isoosmolar effect - water administered with an isosmolar solution (Ringer's solution, Ringer acetate) is distributed between the intravascular and extravascular spaces as 25%: 75% (the volemic effect will be 25% and will last about 30 minutes). These solutions are indicated for isotonic dehydration.

Hypoosmolar effect - more than 75% of the water introduced with the electrolyte solution (disol, acesol, 5% glucose solution) will go into the extravascular space. These solutions are indicated for hypertensive dehydration.

Hyperosmolar effect - water from the extravascular space will enter the vascular bed until the hyperosmolarity of the solution is brought to the osmolarity of the blood. These solutions are indicated for hypotonic dehydration (10% sodium chloride solution) and hyperhydration (10% and 20% mannitol).

Depending on the electrolyte content in the solution, they can be isotonic (0.9% sodium chloride solution, 5% glucose solution), hypotonic (disol, acesol) and hypertonic (4% potassium chloride solution, 10% sodium chloride, 4.2% and 8.4% sodium bicarbonate solution). The latter are called electrolyte concentrates and are used as an additive to infusion solutions (5% glucose solution, Ringer acetate solution) immediately before administration.

Depending on the number of ions in the solution, they are distinguished between monoionic (sodium chloride solution) and polyionic (Ringer's solution, etc.).

The introduction of reserve basicity carriers (hydrocarbonate, acetate, lactate and fumarate) into electrolyte solutions makes it possible to correct violations of metabolic acidosis.

▲ Sodium chloride solution 0.9 % administered intravenously through a peripheral or central vein. The rate of administration is 180 drops/min, or about 550 ml/70 kg/h. The average dose for an adult patient is 1000 ml/day.

Indications: hypotonic dehydration; meeting the need for Na + and O; hypochloremic metabolic alkalosis; hypercalcemia.

Contraindications: hypertensive dehydration; hypernatremia; hyperchloremia; hypokalemia; hypoglycemia; hyperchloremic metabolic acidosis.

Possible complications:

hypernatremia;

hyperchloremia (hyperchloremic metabolic acidosis);

overhydration (pulmonary edema).

g Ringer's acetate solution- isotonic and isoionic solution, administered intravenously. The rate of administration is 70-80 drops/min or 30 ml/kg/h;

if necessary, up to 35 ml/min. The average dose for an adult patient is 500-1000 ml/day; if necessary, up to 3000 ml/day.

Indications: loss of water and electrolytes from the gastrointestinal tract (vomiting, diarrhea, fistulas, drainages, intestinal obstruction, peritonitis, pancreatitis, etc.); with urine (polyuria, isosthenuria, forced diuresis);

Isotonic dehydration with metabolic acidosis - delayed correction of acidosis (blood loss, burns).

Contraindications:

hypertensive overhydration;

• hypernatremia;

  hyperchloremia;

  hypercalcemia.

Complications:

overhydration;

• hypernatremia;

  hyperchloremia.

A Yonosteril- isotonic and isoionic electrolyte solution is administered intravenously through a peripheral or central vein. The rate of administration is 3 ml/kg body weight or 60 drops/min or 210 ml/70 kg/h; if necessary, up to 500 ml/15 min. The average dose for an adult is 500-1000 ml/day. In severe or urgent cases, up to 500 ml in 15 minutes.

Indications:

extracellular (isotonic) dehydration of various origins (vomiting, diarrhea, fistulas, drainages, intestinal obstruction, peritonitis, pancreatitis, etc.); polyuria, isosthenuria, forced diuresis;

Primary plasma replacement for plasma loss and burns. Contraindications: hypertensive overhydration; swelling; heavy

renal failure.

Complications: overhydration.

▲ Lactosol- isotonic and isoionic electrolyte solution is administered intravenously through a peripheral or central vein. The rate of administration is 70-80 drops/min, or about 210 ml/70 kg/h; if necessary, up to 500 ml/15 min. The average dose for an adult is 500-1000 ml/day; if necessary, up to 3000 ml/day.

Indications:

loss of water and electrolytes from the gastrointestinal tract (vomiting, diarrhea, fistulas, drainages, intestinal obstruction, peritonitis, pancreatitis, etc.); with urine (polyuria, isosthenuria, forced diuresis);

isotonic dehydration with metabolic acidosis (rapid and delayed correction of acidosis) - blood loss, burns.

Contraindications: hypertensive overhydration; alkalosis; hypernatremia; hyperchloremia; hypercalcemia; hyperlactatemia.

Complications: overhydration; alkalosis; hypernatremia; hyperchloremia; hyperlactatemia.

▲ Acesol- hypoosmolar solution contains Na +, C1" and acetate ions. Administered intravenously through a peripheral or central vein (stream

or drip). The daily dose for an adult is equal to the daily requirement for water and electrolytes plus "/2 water deficit plus ongoing pathological losses.

Indications: hypertensive dehydration in combination with hyperkalemia and metabolic acidosis (delayed correction of acidosis).

Contraindications: hypotonic dehydration; hypokalemia; overhydration.

Complication: hyperkalemia.

A Sodium bicarbonate solution 4.2% for rapid correction of metabolic acidosis. Administer intravenously undiluted or diluted 5 % glucose solution in a 1:1 ratio, the dosage depends on the ionogram and CBS data. In the absence of laboratory control, no more than 200 ml/day is administered slowly, dropwise. Sodium bicarbonate solution 4.2% should not be administered simultaneously with solutions containing calcium, magnesium, and should not be mixed with phosphate-containing solutions. The dose of the drug can be calculated using the formula:

1 ml of 4.2% solution (0.5 molar) = BE body weight (kg) 0.6.

Indications - metabolic acidosis.

Contraindications- hypokalemia, metabolic alkalosis, hypernatremia.

▲ Osmodiuretics(mannitol). 75-100 ml of 20% mannitol is administered intravenously over 5 minutes. If the amount of urine is less than 50 ml/h, then the next 50 ml are administered intravenously.

9.5.2. Main directions of infusion therapy for hypo- and overhydration

1. Infusion therapy for dehydration should take into account its type (hypertonic, isotonic, hypotonic), as well as:

volume of “third space”; forcing diuresis; hyperthermia; hyperventilation, open wounds; hypovolemia.

2. Infusion therapy for overhydration should take into account its type (hypertonic, isotonic, hypotonic), as well as:

physiological daily need for water and electrolytes;

previous deficiency of water and electrolytes;

ongoing pathological loss of fluid with secretions;

volume of “third space”; forcing diuresis; hyperthermia, hyperventilation; open wounds; hypovolemia.