Symptoms of the disease are disturbances in water metabolism. Dehydration - how dangerous is it? water metabolism disorder

Symptoms of the disease - water metabolism disorders

Violations and their causes by category:

Violations and their causes in alphabetical order:

violation of water metabolism -

The water content in the adult human body is on average 60% of body weight, ranging from 45 (in obese older people) to 70% (in young men). Most of the water (35-45% of body weight) is found inside the cells (intracellular fluid). Extracellular (extracellular) fluid makes up 15-25% of body weight and is divided into intravascular (5%), intercellular (12-15%) and transcellular (1-3%).

During the day, a person drinks about 1.2 liters of water, about 1 liter enters his body with food, about 300 ml of water is formed during the oxidation of nutrients. With normal water balance, the same amount of water (about 2.5 l) is excreted from the body: by the kidneys (1-1.5 l), through evaporation by the skin (0.5-1 l) and lungs (about 400 ml), and is also excreted with feces (50-200 ml).

Two forms are known water metabolism disorders: dehydration of the body (dehydration) and fluid retention in the body (excessive accumulation in tissues and serous cavities).

What diseases cause water metabolism disorders:

I. Dehydration
Dehydration of the body develops due to either limited water intake or excessive excretion from the body with insufficient compensation for lost fluid (dehydration from lack of water). Dehydration can also occur due to excessive loss and insufficient replenishment of mineral salts (dehydration from lack of electrolytes).

1. Dehydration from lack of water intake
In healthy people, restriction or complete cessation of the flow of water into the body occurs under emergency circumstances: among those lost in the desert, among those buried in landslides and earthquakes, during shipwrecks, etc. However, much more often, water deficiency is observed in various pathological conditions:

If there is difficulty swallowing (narrowing of the esophagus after poisoning with caustic alkalis, with tumors, esophageal atresia, etc.);
- in seriously ill and weakened persons (comatose state, severe forms of exhaustion, etc.);
- in premature and seriously ill children;
- for certain brain diseases (idiocy, microcephaly), accompanied by a lack of thirst.

In these cases, dehydration develops from an absolute lack of water.
Throughout life, a person continuously loses water. Mandatory, irreducible water consumption is as follows: the minimum amount of urine, determined by the concentration of substances in the blood to be excreted and the concentrating ability of the kidneys; loss of water through the skin and lungs (lat. perspiratio insensibilis - imperceptible sweating); losses in feces.

In a state of water starvation, the body uses water from water depots (muscles, skin, liver). For an adult weighing 70 kg, they contain up to 14 liters of water. The life expectancy of an adult with absolute fasting without water under normal temperature conditions is 7-10 days.

Children's bodies tolerate dehydration much harder than adults. Under the same conditions, infants lose 2-3 times more fluid per unit of body surface per 1 kg of mass through the skin and lungs. The conservation of water by the kidneys in infants is extremely poor (the concentrating ability of the kidneys is low), and the functional water reserves of a child are 3½ times less than those of an adult. The intensity of metabolic processes in children is much higher. Consequently, the need for water, as well as sensitivity to its lack, is higher compared to an adult organism.

2. Dehydration from hyperventilation. In adults, daily water loss through the skin and lungs can increase to 10-14 liters (under normal conditions this amount does not exceed 1 liter). A particularly large amount of fluid is lost through the lungs in childhood with the so-called hyperventilation syndrome (deep, rapid breathing that continues for a considerable time). This condition is accompanied by the loss of large amounts of water without electrolytes, gas alkalosis. As a result of dehydration and hypersalemia (increased concentration of salts in body fluids), the function of the cardiovascular system is impaired in such children, body temperature rises, and kidney function suffers. A life-threatening condition occurs.

3. Dehydration from polyuria can occur, for example, with diabetes insipidus, congenital polyuria, some forms of chronic nephritis and pyelonephritis, etc.

With diabetes insipidus, the daily amount of urine with low relative density in adults can reach 40 liters or more. If the loss of fluid is compensated, then water metabolism remains in balance, dehydration and disturbances in the osmotic concentration of body fluids do not occur. If fluid loss is not compensated, severe dehydration occurs within a few hours with collapse, fever and hypersalemia.

4. Dehydration from lack of electrolytes
The body's electrolytes, among other important properties, have the ability to bind and retain water. The ions of sodium, potassium, chlorine, etc. are especially active in this regard. Therefore, when the body loses and insufficiently replenishes electrolytes, dehydration develops. Dehydration continues to develop even with free intake of water and cannot be eliminated by the introduction of water alone without restoring the normal electrolyte composition of the body fluids. With this type of dehydration, the body loses water mainly due to extracellular fluid (up to 90% of the volume of lost fluid and only 10% is lost due to intracellular fluid), which has an extremely adverse effect on hemodynamics due to the rapid thickening of the blood.

Loss of electrolytes and water through the gastrointestinal tract. As a result of increased secretion and loss of digestive secretions, the body loses large amounts of electrolytes. With uncontrollable vomiting and diarrhea (gastroenteritis, toxicosis of pregnancy, etc.), the adult body can lose up to 15% of the total amount of sodium, up to 28% of the total amount of chlorine and up to 22% of the total extracellular fluid every day. Large losses of salts and water occur during repeated gastric lavages with liquids that do not contain electrolytes, during continuous pumping of digestive juices, as well as in intestinal, biliary and pancreatic fistulas. Open extensive wounds, burns, weeping eczema and other pathological conditions can lead to significant loss of salts by the body.

Loss of electrolytes and water through the kidneys. Large losses of salts and water through the kidneys can be achieved experimentally by removing the adrenal glands, repeated administration of diuretics, “osmotic” diuresis (administration of urea, hypertonic solutions of glucose, sucrose, mannitol, etc.) and other methods. Large amounts of salts and water can be lost in some forms of nephritis, Addison's disease, etc.

Loss of electrolytes and water through the skin. The electrolyte content of sweat is relatively low. However, with profuse sweating, their loss can reach significant amounts. The daily amount of sweat in a healthy person, depending on environmental temperature factors and muscle load, can range from 800 ml to 10 liters. In this case, sodium can be lost more than 420 mmol/l, and chlorine - more than 150 mmol/l. Therefore, with profuse sweating without adequate intake of salt and water, dehydration is as severe and rapid as with severe gastroenteritis and uncontrollable vomiting. If you try to replace lost water with salt-free liquid, extracellular hypoosmia occurs and water moves into the cells, followed by cellular edema. Symptoms of intracellular edema develop.

II. Water retention in the body
Water retention in the body (overhydration) can occur with excessive water intake (water poisoning) or with limited fluid excretion from the body. In this case, edema and dropsy develop.

1. Water poisoning
Experimental water poisoning can be induced in various animals by loading them with excess water (exceeding renal excretory function) while simultaneously administering antidiuretic hormone (ADH). For example, in dogs, with repeated repeated (up to 10-12 times) injection of water into the stomach, 50 ml per 1 kg of body weight at intervals of 0.5 hours, water intoxication occurs. This causes vomiting, muscle twitching, convulsions, coma and often death.
Excessive water load increases the volume of circulating blood (the so-called oligocythemic hypervolemia, a relative decrease in the content of blood proteins and electrolytes, hemoglobin, hemolysis of erythrocytes and hematuria occurs. Diuresis initially increases, then begins to lag relatively behind the amount of incoming water, and with the development of hemolysis and hematuria occurs true decrease in urine output.

Water poisoning can occur in humans if the intake of water exceeds the ability of the kidneys to excrete it, for example, in some renal diseases (hydronephrosis, etc.), as well as in conditions accompanied by an acute decrease or cessation of urine output (in surgical patients in the postoperative period, in patients in shock, etc.). The occurrence of water poisoning in patients with diabetes insipidus who continued to take large amounts of fluid during treatment with antidiuretic hormonal drugs has been described.

2. Edema
Edema is a pathological accumulation of fluid in tissues and intertissue spaces due to impaired water exchange between blood and tissues. Fluid can also be retained inside cells. In this case, the exchange of water between the extracellular space and cells is disrupted. Such edema is called intracellular. The pathological accumulation of fluid in the serous cavities of the body is called dropsy. The accumulation of fluid in the abdominal cavity is called ascites, in the pleural cavity - hydrothorax, in the pericardial sac - hydropericardium.

Non-inflammatory fluid accumulated in various cavities and tissues is called transudate. Its physicochemical properties differ from those of exudate - inflammatory effusion.
The total water content in the body depends on age, body weight, and gender. In an adult, it makes up about 60% of body weight. Almost 3/4 of this volume of water is inside the cells, the rest is outside the cells. A child’s body contains a relatively larger amount of water, but from a functional point of view, a child’s body is poor in water, since its loss through the skin and lungs is 2-3 times greater than in an adult, and the need for water in a newborn is 120-160 ml per 1 kg of weight, and in an adult 30-50 ml/kg.

Body fluids have a fairly constant concentration of electrolytes. The constancy of the electrolyte composition maintains the constancy of the volume of body fluids and their certain distribution across sectors. A change in the electrolyte composition leads to a redistribution of fluids within the body (water shifts) either to increased excretion or to their retention in the body. An increase in the total water content in the body can be observed while maintaining its normal osmotic concentration. In this case, there is isotonic overhydration. In the case of a decrease or increase in the osmotic concentration of the fluid, they speak of hypo- or hypertonic overhydration. A decrease in the osmolarity of biological body fluids below 300 mOsm per 1 L is called hypoosmia, an increase in osmolarity above 330 mOsm/L is called hyperosmia, or hyperelectrolythemia.

Mechanisms of edema occurrence. The exchange of fluid between vessels and tissues occurs through the capillary wall. This wall is a rather complex biological structure that relatively easily transports water, electrolytes, and some organic compounds (urea), but retains proteins, as a result of which the concentration of the latter in the blood plasma and tissue fluid is not the same (60-80 and 15-30, respectively). g/l). According to the classical theory of Sterling, the exchange of water between capillaries and tissues is determined by the following factors:
1. hydrostatic blood pressure in the capillaries and the value of tissue resistance;
2. colloid osmotic pressure of blood plasma and tissue fluid;
3. permeability of the capillary wall.

Blood moves in the capillaries at a certain speed and under a certain pressure, as a result of which hydrostatic forces are created, tending to remove water from the capillaries into the surrounding tissues. The effect of hydrostatic forces will be greater, the higher the blood pressure, the less resistance from the tissues located near the capillaries. It is known that the resistance of muscle tissue is greater than that of subcutaneous tissue, especially on the face.

The hydrostatic blood pressure at the arterial end of the capillary averages 32 mmHg. Art., and at the venous end - 12 mm Hg. Art. The tissue resistance is approximately 6 mmHg. Art. Therefore, the effective filtration pressure at the arterial end of the capillary will be 32-6 = 26 mmHg. Art., and at the venous end of the capillary - 12 - 6 = 6 mm Hg. Art.

Proteins retain water in the vessels, creating a certain amount of oncotic blood pressure (22 mm Hg). Tissue oncotic pressure is on average 10 mmHg. Art. The oncotic pressure of blood proteins and tissue fluid has the opposite direction of action: blood proteins retain water in the vessels, tissue proteins - in the tissues. Therefore, the effective force (effective oncotic pressure) that retains water in the vessels will be: 22-10 = 12 mm Hg. Art. Filtration pressure (the difference between the effective filtration and effective oncotic pressure) ensures the process of ultrafiltration of liquid from the vessel into the tissue. At the arterial end of the capillary it will be: 26-12 = 14 mm Hg. Art. At the venous end of the capillary, the effective oncotic pressure exceeds the effective filtration pressure and a force equal to 6 mmHg is created. Art. (6-12 = -6 mm Hg), which determines the process of transition of interstitial fluid back into the blood. According to Sterling, there must be an equilibrium here: the amount of fluid leaving the vessel at the arterial end of the capillary must be equal to the amount of fluid passing into the vessel at the venous end of the capillary. However, part of the interstitial fluid is transported into the general bloodstream through the lymphatic system, which Sterling did not take into account. This is a fairly significant mechanism for returning fluid to the bloodstream, and if damaged, so-called lymphedema can occur.

Depending on the causes and mechanism of occurrence, edema is distinguished as cardiac, renal, hepatic, cachectic, inflammatory, toxic, neurogenic, allergic, lymphogenic, etc.

Cardiac, or congestive, edema occurs mainly with venous stagnation and increased venous pressure, which is accompanied by increased filtration of blood plasma and decreased fluid resorption in capillary vessels. Hypoxia that develops during blood stagnation leads to disruption of trophism and increased permeability of the vascular wall. Secondary aldosteronism is also of great importance in the occurrence of cardiac edema in circulatory failure.

Increased venous pressure and blood stagnation that develop with heart failure contribute to the development of edema. Increased pressure in the superior vena cava causes spasm of the lymphatic vessels, leading to lymphatic insufficiency, which further worsens the swelling. An increasing disorder of general circulation may be accompanied by a disorder of the liver and kidneys. In this case, there is a decrease in protein synthesis in the liver and an increase in their excretion through the kidneys, with a subsequent decrease in the oncotic pressure of the blood. Along with this, in heart failure, the permeability of capillary walls increases, and blood proteins pass into the interstitial fluid, increasing its oncotic pressure. All this contributes to the accumulation and retention of water in tissues during heart failure.

Renal edema. In the pathogenesis of edema in glomerulonephritis, primary importance is given to a decrease in glomerular filtration, which leads to water retention in the body. At the same time, sodium reabsorption in the nephron tubules also increases, in which, apparently, a certain role belongs to secondary hyperaldosteronism, since the aldosterone antagonist - spironolactone (a synthetic steroid) gives a diuretic and natriuretic effect in glomerulonephritis. An increase in the permeability of the wall of capillary vessels also plays a known role in the mechanism of development of edema in glomerulonephritis.
In the presence of nephrotic syndrome, the factor of hypoproteinemia (due to proteinuria), combined with hypovolemia, which stimulates the production of aldosterone, comes to the fore.

Nephritic edema. In the blood of patients with nephritis, there is an increased concentration of aldosterone and ADH. It is believed that hypersecretion of aldosterone is caused by a violation of intrarenal hemodynamics with the subsequent activation of the renin-angiotensin system. Angiotensin-2, formed under the influence of renin through a series of intermediate products, directly activates the secretion of aldosterone. In this way, the aldosterone mechanism of sodium retention in the body is mobilized. Hypernatremia (also aggravated by a decrease in the filtration capacity of the kidneys in nephritis) through osmoreceptors activates the secretion of ADH, under the influence of which the hyaluronidase activity of not only the epithelium of the renal tubules and collecting ducts of the kidneys, but also a large part of the capillary system of the body (generalized capillaritis) increases. There is a decrease in water excretion through the kidneys and a systemic increase in capillary permeability, in particular for plasma proteins. Therefore, a distinctive feature of nephritic edema is the high protein content in the interstitial fluid and increased tissue hydrophilicity.

Hydration of tissues is also facilitated by an increase in osmotically active substances (mainly salts) in them by reducing their excretion from the body.

Hypoproteinemia, caused by impaired protein synthesis in the liver, plays an important role in the development of hepatic edema with liver damage. In this case, an increase in the production or disruption of the inactivation of aldosterone is of some importance. In the development of ascites in liver cirrhosis, the decisive role is played by the difficulty of hepatic circulation and the increase in hydrostatic pressure in the portal vein system.

Ascites and edema in liver cirrhosis. In liver cirrhosis, along with local accumulation of fluid in the abdominal cavity (ascites), the total volume of extracellular fluid increases (hepatic edema). The primary point of occurrence of ascites in liver cirrhosis is the difficulty of intrahepatic circulation with a subsequent increase in hydrostatic pressure in the portal vein system. Fluid gradually accumulating inside the abdominal cavity increases intra-abdominal pressure to such an extent that it counteracts the development of ascites. The oncotic pressure of the blood does not decrease until the function of the liver to synthesize blood proteins is impaired. However, when this happens, ascites and edema develop much more quickly. The protein content in ascitic fluid is usually very low. With an increase in hydrostatic pressure in the area of ​​the portal vein, lymph flow in the liver sharply increases. With the development of ascites, fluid transudation exceeds the transport capacity of the lymphatic tract (dynamic lymphatic insufficiency).

An important role in the mechanism of development of general fluid accumulation in liver cirrhosis is played by active sodium retention in the body. It is noted that the sodium concentration in saliva and sweat with ascites is low, while the potassium concentration is high. Urine contains large amounts of aldosterone. All this indicates either an increase in aldosterone secretion or insufficient inactivation of it in the liver with subsequent sodium retention. Available experimental and clinical observations suggest the possibility of both mechanisms.

When the ability of the liver to synthesize albumin is impaired, the oncotic pressure of the blood decreases due to developing hypoalbuminemia, and the oncotic pressure is added to the above factors involved in the development of edema.

Cachectic, or hungry, edema develops with nutritional dystrophy (starvation), malnutrition in children, malignant tumors and other debilitating diseases. The most important factor in its pathogenesis is hypoproteinemia, caused by impaired protein synthesis, and increased permeability of the walls of capillary vessels, associated with impaired trophism.

In the pathogenesis of inflammatory and toxic edema (under the influence of OM, bee stings and other poisonous insects), a primary role is played by impaired microcirculation in the lesion and increased permeability of the wall of capillary vessels. In the development of these disorders, an important role belongs to the released vasoactive substances-mediators: biogenic amines (histamine, serotonin), kinins (bradykinin, etc.), adenosine phosphoric acids, arachidonic acid derivatives (prostaglandins, leukotrienes), etc.

Neurogenic edema develops as a result of a violation of the nervous regulation of water metabolism, trophism of tissues and blood vessels (angiotrophoneurosis). This includes swelling of the extremities with hemoplegia and syringomyelia, swelling of the face with trigeminal neuralgia, etc. In the origin of neurogenic edema, an important role is played by increased permeability of the vascular wall and metabolic disorders in the affected tissues.

Allergic edema occurs due to sensitization of the body and allergic reactions (urticaria, Quincke's edema, allergic rhinitis, swelling of the respiratory tract in bronchial asthma, etc.). The mechanism of development of allergic edema is in many ways similar to the pathogenesis of inflammatory and neurogenic edema. In the resulting disturbances in microcirculation and permeability of the walls of capillary vessels, the leading role is played by the release of biologically active substances.
In the development of edema of various origins, two stages should be distinguished. In the first, excess fluid entering the tissue accumulates mainly in gel-like structures (collagen fibers and the ground substance of connective tissue), increasing the mass of immobile, fixed tissue fluid. When the mass of the fixed fluid increases by approximately 30% and the pressure reaches atmospheric pressure, the second stage begins, characterized by the accumulation of free intercellular fluid. This fluid is able to move under the influence of gravity and gives a “pit sign” when pressure is applied to the swollen tissue.

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– a pathological condition of the human body caused by the action of low temperatures that exceed in intensity the internal reserves of the thermoregulation system. During hypothermia, the temperature of the body's core ( vessels and organs of the abdominal cavity) decreases below optimal values. The metabolic rate decreases, and self-regulation of all body systems fails. In the absence of timely and proportionate care, the lesions progress and can ultimately lead to death.


Interesting Facts

  • When the body temperature drops below 33 degrees, the victim ceases to realize that he is freezing and cannot help himself.
  • Rapidly warming a hypothermic patient can lead to his death.
  • When the skin temperature is less than 10 degrees, its cold receptors are blocked and stop alerting the brain about the danger of hypothermia.
  • According to statistics, every third person who died from hypothermia was intoxicated.
  • Any working skeletal muscle warms up by 2 – 2.5 degrees.
  • The most active areas of the brain are warmer than passive ones, on average, by 0.3 - 0.5 degrees.
  • Shivering increases heat production by 200%.
  • The “point of no return” is considered to be a body temperature of less than 24 degrees, at which it is almost impossible to return a frostbite victim to life.
  • In newborns, the thermoregulation center is underdeveloped.

How is body temperature regulated?

Regulation of body temperature is a complex multi-level process with a strict hierarchy. The main regulator of body temperature is the hypothalamus. This part of the brain receives information from thermoreceptors throughout the body, evaluates it and gives instructions to the intermediary organs for action to implement this or that change. The middle, medulla oblongata and spinal cord exercise secondary control of thermoregulation. There are many mechanisms by which the hypothalamus produces the desired effect. The main ones will be described below.

In addition to thermoregulation, the hypothalamus performs many other equally important functions of the human body. However, to understand the causes of hypothermia, in the future, special attention will be paid only to its thermoregulatory function. To clearly explain the mechanisms of body temperature regulation, it is necessary to trace the development of the body’s response to low temperatures, starting with the excitation of cold receptors.

Receptors

Information about low ambient temperatures is perceived by special cold receptors. There are two types of cold receptors - peripheral ( located throughout the body) and central ( located in the hypothalamus).

Peripheral receptors
There are approximately 250 thousand receptors in the thickness of the skin. Approximately the same number of receptors are found in other tissues of the body - in the liver, gall bladder, kidneys, blood vessels, pleura, etc. Skin receptors are most densely located on the face. With the help of peripheral thermoreceptors, information is collected about the temperature of the environment in which they are located, and a shift in the temperature of the “core” of the body is prevented.

Central receptors
There are significantly fewer central receptors - on the order of several thousand. They are located exclusively in the hypothalamus and are responsible for measuring the temperature of the blood flowing to it. When central receptors are activated, more intense heat generation reactions are triggered than when peripheral receptors are activated.

Both central and peripheral receptors respond to changes in environmental temperature in the range from 10 to 41 degrees. At temperatures outside these limits, the receptors are blocked and stop functioning. An environmental temperature of 52 degrees leads to the destruction of receptors. The transmission of information from receptors to the hypothalamus is carried out through nerve fibers. When the temperature of the environment decreases, the frequency of impulses sent to the brain increases, and when the temperature rises, it decreases.

Hypothalamus

The hypothalamus is a relatively small part of the brain, but it plays an extremely important role in regulating the constancy of the internal environment of the body. Regarding its thermoregulatory function, it should be said that it is conventionally divided into two sections - anterior and posterior. The anterior part of the hypothalamus is responsible for activating heat transfer mechanisms, and the posterior part is responsible for activating heat generation mechanisms. In the hypothalamus there is also a special group of nerve cells that summarizes all the received thermoreceptor signals and calculates the strength of the necessary impact on the body systems to maintain the required body temperature.

When hypothermia occurs, the hypothalamus activates heat production reactions and stops heat loss processes through the following mechanisms.

Heat generation mechanisms

Heat formation, on the scale of the entire organism, is subject to a single rule - the higher the metabolic rate in any organ, the more heat it produces. Accordingly, in order to increase heat generation, the hypothalamus accelerates the work of all organs and tissues. Thus, the working muscle warms up by 2 - 2.5 degrees, the parotid gland - by 0.8 - 1 degree, and actively working areas of the brain - by 0.3 - 0.5 degrees. Acceleration of metabolic processes is carried out by influencing the autonomic nervous system.

The following heat generation mechanisms are distinguished:

  • strengthening muscle work;
  • increase in basal metabolism;
  • specific dynamic effect of food;
  • acceleration of hepatic metabolism;
  • increased heart rate;
  • increase in circulating blood volume;
  • acceleration of the functioning of other organs and structures.
Strengthening muscle work
At rest, striated muscles produce on average 800–1000 kcal per day, which is 65–70% of the heat generated by the body. The body's response to cold is shivering or chills, in which muscles involuntarily contract at a high frequency and low amplitude. Shivering increases heat production by 200%. Walking increases heat generation by 50–80%, and heavy physical work – by 400–500%.

Increase in basal metabolism
Basal metabolism is a value corresponding to the average rate of all chemical reactions in the body. The body's response to hypothermia is to increase basal metabolism. Basic metabolism is not synonymous with metabolism, since the term “metabolism” is characteristic of a single structure or system. In some diseases, the basal metabolic rate may decrease, which ultimately leads to a decrease in comfortable body temperature. The rate of heat generation in such patients is much lower than in other people, which makes them more susceptible to hypothermia.

Specific dynamic action of food
Eating food and digesting it require the body to release some additional amount of energy. Part of it is converted into thermal energy and is included in the general process of heat generation, although only slightly.

Acceleration of liver metabolism
The liver is compared to the chemical factory of the body. Thousands of reactions occur in it every second, accompanied by the release of heat. For this reason, the liver is the “hottest” internal organ. The liver produces an average of 350–500 kcal of heat per day.

Increased heart rate
Being a muscular organ, the heart, like other muscles of the body, generates heat when working. It produces 70–90 kcal of heat per day. When hypothermia occurs, the heart rate increases, which is accompanied by an increase in the amount of heat produced by the heart to 130 - 150 kcal per day.

Increased circulating blood volume
The human body circulates from 4 to 7 liters of blood, depending on body weight. 65 - 70% of the blood is constantly in motion, and the remaining 30 - 35% is in the so-called blood depot ( unused blood reserve needed in emergency situations such as heavy physical work, lack of oxygen in the air, bleeding, etc.). The main blood depots are veins, spleen, liver, skin and lungs. With hypothermia, as indicated above, the basal metabolism increases. An increase in basal metabolism requires more oxygen and nutrients. Since blood is their carrier, its quantity should increase in proportion to the increase in basal metabolism. Thus, blood from the depot enters the bloodstream, increasing its volume.

Acceleration of the functioning of other organs and structures
The kidneys produce 70 kcal of heat per day, the brain - 30 kcal. The breathing muscles of the diaphragm, working continuously, supply the body with an additional 150 kcal of heat. With hypothermia, the frequency of respiratory movements increases from one and a half to two times. Such an increase will lead to an increase in the amount of thermal energy released by the respiratory muscles to 250 - 300 kcal per day.

Mechanisms of heat loss

In conditions of low temperatures, the body's adaptive reaction is to minimize the volume of heat loss. To accomplish this task, the hypothalamus, as in the previous case, acts by influencing the autonomic nervous system.

Mechanisms for reducing heat loss:

  • centralization of blood circulation;
  • increase in subcutaneous fat;
  • reduction of open body area;
  • reduction of heat loss by evaporation;
  • skin muscle reaction.

Centralization of blood circulation
The body is conventionally divided into “core” and “shell”. The “core” of the body is all the organs and vessels of the abdominal cavity. The core temperature practically does not change, since maintaining its constancy is necessary for the correct functioning of vital organs. The “shell” refers to the tissues of the limbs and the entire skin covering the body. Passing through the “shell,” the blood cools, giving energy to the tissues through which it flows. The farther a part of the body is from the “core,” the colder it is. The rate of heat loss directly depends on the amount of blood passing through the “shell”. Accordingly, during hypothermia, to reduce heat loss, the body reduces blood flow to the “shell”, directing it to circulate only through the “core”. For example, at a temperature of 15 degrees, the blood flow in the hand decreases by 6 times.

With further cooling of the peripheral tissue, the blood flow in it may stop completely due to spasm of the blood vessels. This reflex is certainly beneficial for the body as a whole, as it is aimed at preserving life. However, for parts of the body deprived of the necessary blood supply, it is negative, since with prolonged spasm of blood vessels combined with low temperature, frostbite can occur.

Increase in subcutaneous fat
During a long stay in a cold climate, the human body adapts in such a way as to reduce heat loss. The total mass of adipose tissue increases and is redistributed throughout the body more evenly. Its main part is deposited under the skin, forming a layer 1.5 - 2 cm thick. A smaller part is distributed throughout the body and settles between the muscle fascia in the greater and lesser omentum, etc. The essence of this rearrangement is that adipose tissue conducts heat poorly, ensuring its retention inside the body. In addition, adipose tissue does not require such high oxygen consumption. This provides it with an advantage over other tissues in conditions of oxygen deficiency due to prolonged spasm of the vessels feeding it.

Reducing exposed body area
The rate of heat loss depends on the temperature difference and the area of ​​contact of the body with the environment. If it is not possible to influence the temperature difference, then you can change the contact area by taking a more closed position. For example, in cold weather animals curl up into a ball, reducing the area of ​​contact with the environment, and in hot weather, on the contrary, they strive to increase it, straightening up as much as possible. Likewise, a person, falling asleep in a cold room, subconsciously pulls his knees to his chest, taking a more energy-efficient pose.

Reducing heat loss by evaporation
The body loses heat when water evaporates from the surface of the skin or mucous membranes. Scientists have calculated that the evaporation of 1 ml of water from the human body leads to a loss of 0.58 kcal of heat. An adult loses an average of 1400–1800 ml of moisture per day through evaporation during normal physical activity. Of this, 400–500 ml evaporates through the respiratory tract, 700–800 ml through perspiration ( imperceptible seepage) and 300 – 500 ml - through sweat. In conditions of hypothermia, sweating stops, breathing slows down and vaporization in the lungs decreases. Thus, heat loss is reduced by 10 - 15%.

Skin muscle response goose pimples)
In nature, this mechanism occurs very often and consists of tension in the muscles that lift the hair follicles. As a result, the undercoat and cellularity of the coat increase, and the layer of warm air around the body thickens. This results in improved thermal insulation, since air is a poor conductor of heat. In humans, during evolution, this reaction has been preserved in a rudimentary form and has no practical value.

Causes of hypothermia

Factors influencing the likelihood of hypothermia:
  • weather;
  • quality of clothes and shoes;
  • diseases and pathological conditions of the body.

Weather

Parameters that influence the rate of heat loss by the body are:
  • ambient temperature;
  • air humidity;
  • wind power.
Ambient temperature
Ambient temperature is the most significant factor in hypothermia. In physics, in the section of thermodynamics, there is a pattern that describes the rate of decrease in body temperature depending on the temperature of the environment. In essence, it comes down to the fact that the greater the temperature difference between the body and the environment, the more intense the heat exchange occurs. In the context of hypothermia, this rule would sound like this: the rate of heat loss by the body will increase as the ambient temperature decreases. However, the above rule will only work if a person is in the cold without clothes. Clothing greatly reduces heat loss from the body.

Air humidity
Atmospheric humidity affects the rate of heat loss in the following way. As humidity increases, the rate of heat loss increases. The mechanism of this pattern is that at high humidity, a layer of water invisible to the eye forms on all surfaces. The rate of heat loss in water is 14 times higher than in air. Thus, water, being a better conductor of heat than dry air, will transfer body heat to the environment faster.

Wind power
Wind is nothing more than the unidirectional movement of air. In a windless environment, a thin layer of heated and relatively still air forms around the human body. Under such conditions, the body spends a minimum of energy to maintain a constant temperature of this air shell. In windy conditions, the air, barely warmed up, moves away from the skin and is replaced by colder air. To maintain optimal body temperature, the body has to speed up the basal metabolism and activate additional heat generation reactions, which ultimately requires large amounts of energy. At a wind speed of 5 meters per second, the rate of heat transfer increases approximately twofold, at 10 meters per second - fourfold. Further growth occurs in geometric progression.

Quality of clothes and shoes

As mentioned above, clothing can greatly reduce heat loss from the body. However, not all clothing protects against the cold equally effectively. The main influence on the ability of clothing to retain heat is the material from which it is made and the correct selection of the size of the item or shoe.

The most preferred material in the cold season of the year is natural wool and fur. In second place are their artificial analogues. The advantage of these materials is that they have high cellularity, in other words, they contain a lot of air. Being a poor conductor of heat, air prevents unnecessary energy loss. The difference between natural and faux fur is that the cellularity of natural material is several times higher due to the porosity of the fur fibers themselves. A significant disadvantage of synthetic materials is that they contribute to the accumulation of moisture under clothing. As stated earlier, high humidity increases the rate of heat loss, promoting hypothermia.

The size of shoes and clothes should always correspond to body parameters. Tight clothing stretches over the body and reduces the thickness of the layer of warm air. Tight shoes cause compression of the blood vessels that feed the skin, subsequently leading to frostbite. Patients with swollen feet are advised to wear shoes made of soft material that can stretch without compressing the limbs. The sole should be at least 1 cm thick. Large sizes of clothing and shoes, on the contrary, do not fit tightly enough to the body, form folds and crevices through which warm air escapes, not to mention the fact that they are simply uncomfortable to wear.

Diseases and pathological conditions of the body

Diseases and pathological conditions that contribute to the development of hypothermia:
  • cirrhosis of the liver;
  • cachexia;
  • state of alcoholic intoxication;
  • bleeding;
  • traumatic brain injury.
Heart failure
Heart failure is a serious disease in which the pumping function of the heart muscle is affected. The rate of blood flow throughout the body decreases. As a result, the time the blood stays at the periphery increases, which leads to stronger cooling. With heart failure, swelling often forms, starting from the feet and eventually rising higher, up to the chest. Swelling further worsens blood circulation in the extremities and leads to even greater cooling of the blood. To maintain the required body temperature, the body is forced to constantly use heat generation mechanisms, even at normal ambient temperatures. However, when it decreases, the mechanisms of thermogenesis are depleted, and the rate of drop in body temperature increases sharply, introducing the patient into a state of hypothermia.

Cirrhosis of the liver
This disease is the result of long-term replacement of functional liver tissue with non-functional connective tissue. With a long course of the disease, free fluid accumulates in the abdominal cavity, the volume of which can reach 15–20 liters. Since this fluid is located within the body, additional resources must be constantly expended to maintain its temperature and some of the heat generation mechanisms must be involved. The abdomen of such patients is tense. Internal organs and blood vessels are subject to compression. When the inferior vena cava is compressed, edema of the lower extremities rapidly develops. As mentioned earlier, edema leads to additional cooling of the blood, requiring additional efforts of the heat generation system. As the ambient temperature decreases, the heat generation mechanisms will no longer cope with their task, and the patient’s temperature will begin to steadily fall.

Addison's disease
Addison's disease is adrenal insufficiency. Normally, the adrenal cortex produces three types of hormones - crystalloids ( aldosterone), glucocorticoids ( cortisol) and androgens ( androsterone). If there is insufficient amount of two of them in the blood ( aldosterone and cortisol) blood pressure decreases. A decrease in blood pressure leads to a slowdown in the speed of blood flow throughout the body. Blood passes one circle through the human body over a longer period of time, cooling more strongly. In addition to the above, a lack of glucocorticoids leads to a decrease in the body's basal metabolism, a decrease in the rate of chemical reactions accompanied by the release of energy. As a result, the core produces less heat, which, coupled with greater cooling of the blood, leads to a significant risk of hypothermia, even at moderately low temperatures.

Hypothyroidism
Hypothyroidism is an endocrine disease caused by insufficient production of thyroid hormones. Like glucocorticoids, thyroid hormones ( triiodothyronine and thyroxine) are responsible for the regulation of many biological processes in the human body. One of the functions of these hormones is to maintain a uniform rate of reactions accompanied by the release of heat. When thyroxine levels decrease, body temperature decreases. The more pronounced the hormone deficiency, the lower the constant body temperature. Such patients are not afraid of high temperatures, but in the cold they quickly become hypothermic.

Cachexia
Cachexia is a state of extreme exhaustion of the body. It develops over a relatively long time ( weeks and even months). The causes of cachexia are cancer, AIDS, tuberculosis, cholera, prolonged malnutrition, extremely high physical activity, etc. With cachexia, the patient’s weight is greatly reduced, mainly due to fat and muscle tissue. This is what determines the mechanism for the development of hypothermia in this pathological condition. Adipose tissue is a kind of thermal insulator of the body. With its deficiency, the rate of loss of body temperature increases. In addition, adipose tissue, when broken down, produces 2 times more energy than any other tissue. In its absence, the body has to use proteins for its own heating - the “building blocks” from which our body is built.

The above situation can be compared with heating a residential building by oneself. Muscles are the main structure of the body that produces thermal energy. Their share in heating the body is 65–70% at rest, and up to 95% during intensive work. As muscle mass decreases, the level of heat production by the muscles also decreases. Summarizing the effects obtained, it turns out that a decrease in the thermal insulating function of adipose tissue, its absence as the main source of heat generation reactions and a decrease in the mass of muscle tissue leads to an increase in the risk of hypothermia.

State of alcoholic intoxication
This condition is a consequence of a certain amount of alcohol in a person’s blood, which can cause a certain biological effect. According to scientists, the minimum amount of alcoholic drink required to begin the development of inhibition processes of the cerebral cortex ranges from 5 to 10 ml of pure alcohol ( 96% ), and for dilating the blood vessels of the skin and subcutaneous fat, it ranges from 15 to 30 ml. For the elderly and children, this measure is half as much. When peripheral vessels dilate, a deceptive sensation of warmth is created.

It is with this effect of alcohol that the myth is associated that alcohol helps to warm the body. By dilating blood vessels, alcohol prevents the manifestation of the centralization reflex of blood circulation, developed over millions of years of evolution, and designed to preserve human life in low temperatures. The catch is that the feeling of warmth is caused by the flow of warm blood from the torso to the cold skin. The incoming blood quickly cools and returning to the “core” greatly reduces the overall body temperature. If a person in a state of severe alcoholic intoxication falls asleep on the street at sub-zero temperatures, then most often he wakes up in a hospital room with frostbitten limbs and bilateral pneumonia, or does not wake up at all.

Bleeding
Bleeding is the flow of blood from the bloodstream into the external environment or into the body cavity. The mechanism of action of blood loss leading to hypothermia is simple. Blood is a liquid medium that, in addition to oxygen and nutrients, transfers thermal energy to organs and tissues. Accordingly, the body's loss of blood is directly proportional to the loss of heat. Slow or chronic bleeding is tolerated much better by humans than acute bleeding. With prolonged slow bleeding, the patient can survive even after losing half of his blood.

Acute blood loss is more dangerous, since it does not have time to activate compensatory mechanisms. The severity of the clinical picture of acute bleeding depends on the volume of blood loss. Blood loss of 300–500 ml is tolerated by the body almost imperceptibly. Blood reserves are released, and the deficiency is completely compensated. With blood loss of 500 to 700 ml, the victim experiences dizziness, nausea, and a strong feeling of thirst. There is a need to take a horizontal position to alleviate the condition. Blood loss of 700 ml - 1 liter is manifested by a short-term loss of consciousness. When a victim falls, his body assumes a horizontal position, blood is directed to the brain, and the person comes to his senses on his own.

The most dangerous is acute blood loss of more than 1 liter, especially in conditions of negative temperatures. The patient may lose consciousness for a period of half an hour to several hours. While he is unconscious, all thermoregulation mechanisms are turned off. Thus, the rate of drop in body temperature of an unconscious person is equal to the rate of drop in body temperature of a corpse, which on average equals one degree per hour ( in the absence of wind and normal air humidity). At this rate, a healthy person will reach the first degree of hypothermia in 3, the second in 6–7 and the third in 9–12 hours.

Traumatic brain injury
With a traumatic brain injury, as with heavy bleeding, there is a risk of loss of consciousness. The danger of hypothermia during loss of consciousness is described in detail above.

Degrees of hypothermia

Classification of stages of hypothermia depending on clinical manifestations

Stage Development mechanism External manifestations
Dynamic Spasm of peripheral vessels. Compensatory activation of all heat generation mechanisms. Excessive stress activation of the sympathetic autonomic nervous system. Pale skin, goose bumps.
Severe muscle tremors. The ability to move independently is preserved.
Lethargy and drowsiness, slow speech, slow reaction to stimuli.
Rapid breathing and heart rate.
Stuporous Depletion of the body's compensatory reactions. Deterioration of peripheral blood supply, up to its absence. Slowing down metabolic processes in the brain. Partial separation of the activity of the cortex and subcortical zone. Suppression of the brain centers of breathing and heartbeat. Paleness of the skin. Ears, nose, cheeks, limbs become bluish in color. Associated frostbite of 1 – 2 degrees.
No muscle tremors. Muscle stiffness, up to the inability to straighten the limb. Boxer pose.
Superficial coma. The pupils are moderately dilated, the reaction to light is positive. Reaction only to strong painful stimuli.
Breathing slows down and becomes shallow. Decrease in heart rate.
Convulsive Complete depletion of compensatory mechanisms.
Damage to peripheral tissues due to prolonged lack of blood supply.
Extreme deterioration of metabolic processes in the brain. Complete separation of the work of different parts of the brain. The appearance of foci of convulsive activity.
Severe depression of the brain centers of breathing and heartbeat.
Slowdown of the conduction system of the heart.
Pale blue skin. Associated frostbite of 3 – 4 degrees of protruding parts of the body.
Severe muscle rigor.
Deep coma. The pupils are maximally dilated. The reaction to light is absent or extremely weak. There is no reaction to any stimuli.
Attacks of generalized convulsions are repeated every 15 to 30 minutes.
Lack of rhythmic breathing. Reducing heart rate to 20 - 30 per minute. Rhythm disturbances. At 20 degrees, breathing and heartbeat usually stop.


Due to the fact that the stages of clinical manifestations of hypothermia do not always correspond to certain temperature limits, there is a classification of degrees of hypothermia depending on body temperature that is of secondary clinical information value.

Classification of degrees of hypothermia, depending on body temperature

Symptoms of hypothermia

In this section, the symptoms of hypothermia are selected in such a way that the victim or first aid provider can roughly determine the severity of hypothermia without specialized equipment.

Symptoms of hypothermia in order of appearance

Symptom Reason for appearance
Pale skin Spasm of peripheral vessels to reduce heat transfer.
"Goose pimples A rudimentary defensive reaction in the form of tension in the muscles that lift the hair follicle. In animals it helps to increase the undercoat layer. It has no effect in humans.
Shiver Rhythmic contractions of muscle fibers, characterized by high frequency and low amplitude. Lead to an increase in heat production up to 200%.
Tachycardia A compensatory reaction of the body to a threat caused by excessive tone of the sympathetic nervous system and an increase in the level of adrenaline in the blood.
Rapid breathing At low temperatures, the body is forced to speed up the basal metabolism and activate heat production systems. These processes require increased oxygen delivery, which is carried out through increased breathing.
Weakness, drowsiness Cooling the blood leads to slow cooling of the brain. Cooling of the reticular formation, a special structure of the brain, leads to a decrease in the tone of the body, which is felt by a person as lethargy, weakness and a craving for sleep.
Rigor Freezing of a muscle causes it to lose its ability to excite. In addition, the rate of metabolic processes in it drops to almost zero. Intracellular and intercellular fluids crystallize.
Pain The appearance of pain is associated with the process of tissue hardening during freezing. When in contact with rough tissue, pain receptors are excited much more strongly than when in contact with soft tissue. Increased impulses of the excited nerve create a sensation of pain in the brain.
Slow reaction and speech The slowing of speech is associated with a decrease in the activity of the speech center of the brain due to its cooling. The slowing down of the reaction is caused by a decrease in the speed of passage of the nerve impulse along the reflex arc ( the path from its formation to the effects caused by it).
Decreased heart rate The cause of this symptom is a decrease in the activity of the heartbeat center located in the medulla oblongata.
Decreased respiratory rate This phenomenon occurs due to a decrease in the activity of the respiratory center located in the medulla oblongata.
Spasm of the masticatory muscles (trismus) This symptom is similar in origin to rigor in other muscles of the body, but it brings much more trouble. Trismus usually develops in the stuporous and convulsive stages of frostbite. Carrying out resuscitation measures involves inserting a plastic tube into the patient’s airway, but due to trismus, this manipulation cannot be performed.
Convulsions When the temperature of the brain drops below 28 degrees, the synchronous functioning of all its departments is disrupted. Foci of asynchronous impulses are formed, characterized by high convulsive activity.
Pathological breathing This type of breathing is represented by periods of increasing and decreasing depth of breathing, interrupted by long pauses. The effectiveness of such breathing is extremely low. This indicates cold damage to the respiratory center located in the brain stem and means a poor prognosis for the patient.
Heart rhythm disturbances The first reason is the inhibition of the heartbeat center mentioned above. The second reason is disruption of the processes of excitation and conduction of nerve impulses in the heart itself. As a result, additional foci of excitation arise, leading to arrhythmias, and impulse conduction blocks leading to asynchronous contraction of the atria and ventricles. Any of these rhythm disturbances can lead to cardiac arrest.
Lack of breathing and heartbeat This symptom develops when the body temperature is below 20 degrees. It is a consequence of extreme inhibition of the corresponding centers of the brain. Requires chest compressions and artificial respiration.

First aid for hypothermia

It is extremely important, before starting first aid, to determine the severity of hypothermia and decide whether there is a need to call an ambulance.

Indications for hospitalization for hypothermia:

  • stuporous or convulsive stage of general hypothermia;
  • poor response to first aid even during the dynamic stage of hypothermia;
  • concomitant frostbite of body parts of III and IV degrees;
  • concomitant frostbite of parts of the body I and II degrees in combination with vascular diseases of the lower extremities or diabetes mellitus.

After assessing the severity of the victim and, if necessary, calling an ambulance, the patient should be given first aid.

Algorithm for action in case of hypothermia:

  1. Stop the victim's contact with the cold environment. It is necessary to take him to a warm room, remove frozen and wet clothes and change into clean, dry clothes.
  2. Offer the victim any warm drink ( tea, coffee, broth). It is important that the temperature of the drink does not exceed body temperature by more than 20 - 30 degrees, otherwise the risk of burns to the oral mucosa, esophagus and stomach increases.
  3. Wrap the patient in any thermal insulating material. The most effective in this case will be special blankets made of thick foil. In their absence, you can use cotton blankets or any other.
  4. Avoid excessive movement of the victim from place to place, as unnecessary movements can cause pain and contribute to heart rhythm disturbances.
  5. Body massage in the form of light rubbing promotes heat generation through friction, and also accelerates the restoration processes of the skin and subcutaneous tissue. However, rough massage can provoke the heart rhythm disturbances mentioned above.
  6. Warm baths bring a good therapeutic effect. The water temperature at the beginning of the procedure should be equal to body temperature or exceed it by 2 - 3 degrees. Then you should slowly increase the water temperature. The temperature rise should not exceed 10 - 12 degrees per hour. It is extremely important to monitor the patient’s condition during active warming in a warm bath, since with rapid warming, there is a possibility of developing “Afterdrop” syndrome, in which blood pressure drops sharply, leading to a state of shock.
First aid medications for hypothermia:
  • Antispasmodics. This group of medications should be used only after the victim has begun to warm up. Prescribing them to a patient under the influence of cold will sharply worsen his condition. The rate of decrease in temperature will increase and an earlier decrease in respiratory rate will develop than would occur without the prescription of the drug. Papaverine 40 mg 3 – 4 times a day is used as antispasmodics; drotaverine ( no-shpa) 40 – 80 mg 2 – 3 times a day; mebeverine ( duspatalin) 200 mg 2 times a day.
  • Painkillers. Pain is a factor that in itself contributes to the worsening of any disease. The presence of pain during hypothermia is a direct indication for the use of painkillers. Analgin 500 mg 2-3 times a day is used as an analgesic for hypothermia; dexketoprofen 25 mg 2 – 3 times a day; ibuprofen 400 mg 4 times a day.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs). This group of drugs is used to prevent inflammatory processes after warming up the victim, as well as to reduce the intensity of pain. For stomach and duodenal ulcers, this group of drugs is used with caution. The following non-steroidal anti-inflammatory drugs are used to treat hypothermia: acetylsalicylic acid ( aspirin) 250 – 500 mg 2 – 3 times a day; nimesulide 100 mg 2 times a day; ketorolac ( ketanov) 10 mg 2 – 3 times a day.
  • Antihistamines. This group of drugs is actively used for allergic diseases. However, they are no less effective in fighting any inflammatory process of non-bacterial origin, and accordingly are suitable for reducing the symptoms of hypothermia. The most common antihistamines are: suprastin 25 mg 3–4 times a day; clemastine 1 mg 2 times a day; Zyrtec 10 mg once a day.
  • Vitamins. The most effective drug in case of hypothermia is vitamin C. Its positive effect is to strengthen the walls of blood vessels damaged by low temperatures. It is used 500 mg 1 – 2 times a day.
The above drugs are given in doses corresponding to an adult without significant impairment of the excretory function of the kidneys. If adverse reactions occur to any of the medications taken, you should immediately seek qualified medical help.

Treatment of hypothermia

Treatment of hypothermia is an extremely difficult task, as it requires a broad approach to the pathology. With hypothermia, disruptions in the functioning of all body systems occur, and assistance must be provided in a comprehensive manner, otherwise treatment will lead to nothing. It is also important to note that treatment of hypothermia at home is only permissible for the first ( dynamic) its stages. In the stuporous and convulsive stages, treatment in a hospital in the intensive care unit is necessary.

Attempts to treat a patient with hypothermia of the second and third stages at home are doomed to failure for at least three reasons. Firstly, at home there is no special equipment and laboratory in order to constantly monitor the dynamics of changes in the body’s vital signs. Secondly, the condition of such patients requires intensive supportive therapy, in the absence of which the patient cannot recover using only his own body. Thirdly, the condition of a patient with hypothermia tends to sharply deteriorate, which in the absence of appropriate assistance will lead to his quick and inevitable death.

Once in the hospital emergency room, a victim of hypothermia is immediately sent to the intensive care unit ( resuscitation). The main therapeutic measures are divided into two main areas - warming the patient and correcting the vital signs of the body.

Warming the victim:

  • Eliminate contact of frozen clothing with the victim’s body.
  • Wrapping the victim in a thermal insulating material, such as a special “space” blanket, the main component of which is foil.
  • Place the patient under a lamp with dosed infrared radiation.
  • Covering the patient with heating pads with warm water. The water temperature in them should not exceed body temperature by more than 10 - 12 degrees.
  • Immersion in a warm bath. The water temperature at the beginning of the procedure is 2–3 degrees higher than body temperature. Subsequently, the water temperature rises by 8 - 10 degrees per hour.
  • Applying heat to the projections of large blood vessels.
  • Intravenous administration of warm infusion solutions, the temperature of which should not exceed 40 - 42 degrees.
  • Gastric lavage with warm water ( 40 – 42 degrees). If there is spasm of the masticatory muscles and it is impossible to insert the probe through the mouth, diazepam is injected into the muscles of the floor of the mouth, and then the probe is reinserted. If there is spasm in the masticatory muscles, you can insert a probe through the nose ( nasogastric tube), however with great caution, as the risk of vomiting and stomach contents entering the respiratory tract significantly increases.
Correction of vital signs:
  • Oxygenation with humidified oxygen. The percentage of oxygen in the inspired air should be selected so that the saturation ( saturation) blood oxygen was more than 95%.
  • Maintaining blood pressure within 80/60 – 120/80 mmHg. For low blood pressure, atropine 0.1% - 1 ml is administered intravenously ( diluted with 10 – 20 ml saline); prednisolone 30 – 60 mg; dexamethasone 4 – 8 mg.
  • Correction of the electrolyte composition of the blood - Ringer-Lock solution, Ringer-lactate, dextran-40, dextran-70, etc.
  • Correction of blood glucose levels - glucose 5, 10 and 40%; insulin.
  • Artificial ventilation is used for extremely severe hypothermia, when the victim is unable to breathe on his own.
  • An external cardioverter and defibrillator are used when serious heart rhythm disturbances occur. The cardioverter artificially causes contraction of the heart muscle when an excessively long pause occurs. A defibrillator is used when ventricular fibrillation and pulseless tachycardia occur.
  • An electrocardiograph is used continuously to monitor cardiac activity.
When the patient's condition improves and the threat to life disappears, he is transferred to the general therapy department or any other department at the discretion of the attending physician for further recovery.

Prevention of hypothermia

Practical recommendations:
  • Clothes should be warm and dry, preferably made from natural materials.
  • Open parts of clothing must be tightened as tightly as possible to prevent air from entering under them.
  • A hood is an extremely useful piece of clothing, as it significantly improves head protection from wind, rain and snow.
  • It is necessary to find natural shelter from the wind, for example, cliffs, caves, walls of buildings and entrances. Good protection from the wind can be achieved by constructing a canopy of branches, or simply burying yourself in a pile of leaves or a haystack. In order not to suffocate, it is necessary to provide a small hole for ventilation.
  • Shoes must match your foot size. The sole must be at least 1 cm thick.
  • Active movements such as squats and running in place increase heat production and reduce the chances of hypothermia.
  • If possible, it is necessary to drink hot drinks as often as possible.
  • Alcohol is contraindicated for consumption in cold weather as it increases heat transfer.
  • In cold weather, it is necessary to provide the diet with a large amount of fats and carbohydrates, as well as introduce additional meals into the daily routine.
  • An external heat source, such as a fire, greatly increases your chances of avoiding hypothermia.
  • If necessary, it is necessary to ask passers-by for help and stop passing cars.

Many people have no idea what dehydration actually is, the symptoms of which are quite easy to identify.

As soon as the first signs of this deviation appear, it is necessary to immediately begin to correct the situation so that the person’s condition does not worsen and the consequences of dehydration do not begin to develop.

Causes of dehydration

The most common factor that leads to this condition is a long period when water does not enter the body. But there are other causes of dehydration.

For example, there are many diseases that have symptoms associated with a lack of fluid in the human body. For example, such diseases are acute forms of various pathological processes in the organs of the digestive system. Most often this happens if a person has liquid stool. Then it loses a significant amount of moisture. The same thing happens with vomiting attacks. When a person vomits, he loses moisture from the esophagus and stomach, and dehydration occurs even faster with diarrhea. Various infectious diseases can also lead to dehydration. This happens because a person's body temperature rises, he begins to sweat and loses moisture. In addition, water exits through the respiratory tract in the form of phlegm and mucus.

In addition to diseases, dehydration can be caused by various drinks. For example, many sodas, tea, beer, coffee and spirits contain more than just water. They contain small doses of chemicals that speed up the process of removing fluid from the body. As a result, if you drink them, the body receives less water. By the way, almost all people with colds and other diseases of the respiratory system try to drink as much hot tea as possible. In fact, it causes a person to sweat more, and then the body loses fluid again.

Dehydration can be caused by the use of various medications. In order for the body to absorb any substance, it requires water. So you shouldn’t be surprised that during the treatment of any disease the patient loses even more moisture. Dehydration after such procedures must be treated immediately, otherwise the treatment process will take a long time.

Types and degrees of dehydration

There are several types of dehydration. The first type is hypertensive. It characterizes severe dehydration in a person. It is known as intracellular. It arises from direct loss of fluid, for example, after diarrhea, vomiting, hyperhidrosis and other pathological diseases. There is a hypotonic type of dehydration. It is also called extracellular or hypoosmatic. This condition occurs when a person loses a significant amount of electrolytes compared to the lack of water. Most often this occurs due to vomiting. In this case, the osmotic type of blood fluid concentration begins to drop sharply. There is also an isotonic type of dehydration. It occurs if the body loses a proportionate amount of both moisture and electrolytes.

There are also different degrees of dehydration. They are calculated to establish the ratio of a person's weight before diarrhea or vomiting and after these symptoms. There are 3 degrees of severity of the disease. The first degree is considered easier. In this case, the person’s weight is reduced to 5%. In the second stage, which is known as the middle stage, a person loses no more than 9% of his own weight. At the most severe stage of dehydration, he may lose more than 9% of his body weight. If about 20% of water in relation to body weight is lost from the human body, then various metabolic disorders develop. If this ratio is more than 20%, then death is possible.

If there is no clear data on a person’s weight before the onset of dehydration, then the degree of development of the pathology can be determined by clinical signs and indicators. For example, a mild form of dehydration is considered the most common in children after diarrhea. It occurs in 90 percent of all cases with this pathology. The main symptom in this case is intense thirst. A person can only lose 2% of their own weight. Despite the lack of moisture, the eyes and mouth will be moisturized, so that their mucous membranes will not be damaged. Vomiting attacks occur rarely, and attacks of diarrhea occur every 6-7 hours.

With the second degree of dehydration, which is considered the moderate form, the stool becomes mushy. Weight loss will be up to 9% of the initial value. Moreover, that form develops in 1-2 days. You may find leftover food in your stool that has not been digested. There may be a urge to defecate up to 10 times a day. Vomiting at this stage is already becoming quite common. If a person has lost a total of 7% of body weight in water, he will experience mild dryness and thirst. Dryness will also apply to the mucous membranes of various organs. In addition, the patient experiences mild anxiety. The pulse becomes unstable and the heart rate increases. When the weight loss rate reaches 9%, all signs of dehydration become more obvious. The saliva will be very viscous, the skin will no longer be elastic, and its tone will be lost. Muscle tone begins to deteriorate. The foreground fontanel begins to sink. The eyes become soft. The skin takes on a bluish tint. Urinary excretion becomes insufficient. Symptoms appear that the tissue circulation process is disrupted.

The most severe form of the disease develops when a person passes liquid stool more than 10-12 times a day. Vomiting at this stage becomes constant. Many people know what dehydration is, the symptoms of which are not so striking. However, the later stages are very dangerous for humans, so it is better not to delay treatment of the pathology. Weight loss will be more than 10% of the total weight. The membranes in the mouth feel dry when they are no longer smooth and elastic. If you pull it a little or pinch it, it takes a very long time to restore it to its previous state. Facial expressions cease to exist on a person’s face. The eye sockets are strongly sunken. By the way, the eyes also feel excessively dry. The skin is called marbled. Blood pressure ratios begin to slowly fall. Signs of a white spot appear if the patient is dehydrated, the symptoms of which are quite severe. There will be a small amount of urine when urinating. Acidosis develops. The heartbeat accelerates greatly. As a result, the patient experiences a state of shock. This is because the volume of blood that needs to circulate throughout the body is reduced.

Symptoms of dehydration

Dehydration can manifest differently in adults and children. In addition, the manifestation of this disease is influenced by the degree, types and forms of the disease. For example, if a patient has a hypertensive form of dehydration, it will develop rapidly. By the way, dehydration in a child will manifest itself less actively at the very beginning. In the hypertensive form of the disease, the onset of its manifestation will be very sharp and acute for the patient, and the course of this form of the disease will also remain very stormy. First, the person will feel thirsty. He feels dry in his mouth and nose. Then there is lethargy, fatigue, fatigue, lack of desire to do anything, complete apathy, which can be replaced by irritability or another type of excitement. But then the patient will again experience a loss of strength. In some cases, muscle spasms are noticeable. Consciousness becomes confused. Possible fainting. The state of coma progresses. The skin becomes sluggish, tight and dry. The patient has hyperthermia. When urinating, insufficient moisture is released, and the urine will become more concentrated. The amount of moisture in the blood also decreases. In some cases, tachycardia develops. The patient's breathing becomes rapid.


With the hypotonic type of dehydration, the disease itself will develop quite slowly. This happens because the person is constantly vomiting and this is the main reason. The main signs of the disease are considered to be a decrease in skin firmness, elasticity, and density. In addition, the moisture content of the epithelium also begins to gradually decrease. All these trends also apply to the condition of the eyeballs. Signs of a circulatory disorder are noticeable. In the blood fluid, when diagnosing the condition of the human body, it will be possible to see that the content of nitrogen-type metabolites has increased. The functionality of the kidneys is gradually impaired. The same processes occur in the patient’s brain. When analyzing the blood fluid, you will notice that the amount of moisture that should be contained in it has decreased. By the way, with the hypotonic type of dehydration, a person does not feel thirsty, and water or other drinks cause him not only nausea, but also vomiting attacks. The contractility of the heart gradually fades, but the heartbeat accelerates. A little later, shortness of breath develops, and in more severe forms, suffocation.

With the isotonic type of dehydration, the patient will experience manifestations of the disease, but they will be more moderate. Signs begin to appear that the person has metabolic problems. The heart rate increases. By the way, when listening, it will be possible to determine that the tones of the heart become duller than they should be in a person without loss of moisture in the human body.

Diagnosis and treatment of human dehydration

To determine the level of dehydration, its form and extent, it is necessary to pay attention to the symptoms. In addition, several laboratory tests should be performed to confirm the diagnosis. For example, the most important data will be obtained not from examining the patient himself, but from conducting tests that will help determine the degree of thickness of the blood fluid. This way it will be possible to determine how much water is lost from the patient’s blood. Then it is imperative to pay attention to the quantitative indicator of red blood cells and their frequency per certain volume of liquid. In addition, it is very important to study the amount of electrolytes contained in the plasma, and then establish their concentration indicator.

There are many developed medications that a doctor prescribes when diagnosing dehydration. If a person has a more severe form of the disease, he has signs of a hypovolemic crisis, then he is prescribed albumin and other similar drugs. This requires the introduction of sols one at a time. This is necessary in order to restore blood circulation and its volume, as well as improve fluid circulation in the intercellular space. In addition, the patient is administered various solutions that contain salts and glucose. The doctor must constantly monitor the volumes and concentrations of all fluids that enter the body through the veins. What solutions need to be infused - dextrose or saline - is determined by the doctor based on the type of dehydration of the patient. It is necessary to pay attention to whether the patient has a lack of moisture or electrolytes.

The patient can be treated with both oral and parenteral methods. This depends on the degree of dehydration, the patient's age and metabolic problems. For example, if the patient has the first degree of the disease, then oral medications are prescribed. This may also be acceptable in some cases of the second degree of severity of the disease. In this case, solutions that contain salts and glucose are used. Also, for oral treatment, solutions that do not contain salts are prescribed. For example, light tea is suitable for the patient. You can add lemon slices to it. In addition, you can brew various decoctions and make tinctures of various herbs that treat the condition of lack of moisture in the body. You can drink decoctions based on some vegetables and cereals. These are traditional medicine that have long been time-tested. In addition, various juices from vegetables and fruits are suitable for the patient. They must be fresh. In this case, the juice must be mixed with clean water in equal proportions, otherwise it will not be able to be absorbed in the body. Regular compotes will also work. You are allowed to drink mineral water.

Water is the second most important substance after oxygen, necessary for chemical and metabolic processes in the human body. That is why dehydration of the body can provoke the occurrence of various diseases and pathologies. Against this background, various endocrine, cardiovascular, muscular and mental diseases develop.

Causes of dehydration

Dehydration of the body is primarily caused by an excess of water being removed from it compared to its intake. Lack of water provokes the emergence of a variety of diseases. For example, water lubricates joints and participates in the processes of digestion and respiration, since human lungs need continuous hydration in order to free the blood from carbon dioxide and saturate it with oxygen.

Basically, dehydration occurs due to dry air that enters the lungs. The first reaction to this is increased urination, which means a significant loss of not only fluid, but also sodium chloride, which leads to disturbances in water-salt metabolism.

Blood that has lost the required amount of water decreases in volume and begins to circulate more slowly, which leads to excessive stress on the heart. Thus, the body loses the ability to get rid of excess heat in hot conditions and distribute it in cold times.

It has been established that the body needs up to 3 liters of fluid per day to maintain water balance, and in the hot season this amount increases. Therefore, its deficiency can provoke dehydration of the body. If the air temperature exceeds +35°C, the human body begins to heat up, especially during any physical activity. Maintaining a normal temperature and getting rid of excess heat is achieved through sweating. During this process, a person loses a lot of fluid, which must be restored. If the required amount of moisture is not restored, such losses lead to its deficiency.

The main reasons for lack of water in the human body are:

  • Intense sweating;
  • Increased urination;
  • Severe nausea and vomiting;
  • Acute diarrhea;
  • Insufficient fluid intake caused by loss of appetite or vomiting.

Symptoms of dehydration

The first symptom of dehydration is, naturally, an increased feeling of thirst, however, it does not manifest itself in everyone from the very beginning of this pathological process. The surest sign of its presence is a change in the color and quantity of urine: if its volume has decreased significantly and the color has become dark yellow, this indicates a lack of fluid in the human body and the need to replenish it.

In addition, sure signs of dehydration are severe sweating at high temperatures and physical exertion, dark circles under the eyes, a noticeable decrease in activity, fatigue and various disturbances in the functioning of the senses.

It is known that a lack of fluid primarily has a negative effect on the brain, since it consists of 85% water. In conditions of its shortage, energy production in the brain sharply decreases, which greatly affects the senses. That is why among the symptoms of dehydration the following should be highlighted:

  • Irritability and restlessness;
  • Dejection and depression;
  • Weakening of sexual desire;
  • Heaviness in the head and headaches;
  • Food addictions, cravings for alcohol, smoking and drugs.

All these signs of dehydration may indicate the initial stage of depression, which can trigger the development of chronic fatigue in a person. According to some experts, lack of water in the brain tissue is a direct cause of continuous social stress, accompanied by feelings of self-doubt, fear, anxiety and other emotional problems.

The most serious symptoms of dehydration that develop if the required amount of fluid is not restored are:

  • General weakness;
  • Confusion leading to fainting;
  • Grayness and flabbiness of the skin;
  • Convulsions;
  • Tachycardia.

These indicators of water deficiency, left unattended, often lead to complications such as kidney damage, shock, and even death.

Treatment of dehydration

Experts note that dehydration is easier to prevent than to treat. Therefore, regardless of activity level and health status, it is necessary to drink the maximum amount of fluid throughout the day. The risk group primarily includes young children and older people, especially with attacks of nausea and vomiting, diarrhea and fever.

Treatment for dehydration involves drinking water constantly, but if you lose electrolytes, you need to replace the lack of sodium and potassium. To restore salts, there are special formulations such as glucosolan or citraglucosolan, which can be used both for prevention and for mild dehydration. It is recommended to add a little salt to your drinking water during or after heavy physical activity. However, this method is considered effective only if you drink a lot of water during the day.

When fluid deficiency leads to a significant decrease in blood pressure, which poses a threat to life, solutions containing sodium chloride are administered intravenously. In addition, to treat dehydration, it is necessary to eliminate the cause that provoked it. For example, for diarrhea, in addition to restoring the required amount of water, you should take medications that correct stool. If the kidneys excrete a lot of water, treatment with a synthetic hormone may be needed.

After eliminating the cause of dehydration, it is necessary to monitor fluid intake and prevent relapses. To do this, it is recommended for an adult to drink at least 2-3 liters of water daily, especially in hot weather and during significant physical activity.

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  • 2.2. The harmful effects of sounds and noise
  • 2.3. Effect of barometric pressure
  • 2.3.1. Effect of low barometric pressure. Mountain (altitude) sickness
  • 2.3.2. The effect of increased barometric pressure. Caisson disease
  • 2.4. The pathogenic effect of low temperature. Hypothermia
  • 2.5. The pathogenic effect of thermal energy. Overheating. Heatstroke
  • 2.6. Damaging effects of solar spectrum rays
  • 2.6.1. Effect of ultraviolet radiation
  • 2.6.2. Damaging effects of laser radiation
  • 2.7. The harmful effects of electric current
  • 2.8. Damaging effects of ionizing radiation
  • 2.8.1. General characteristics of the damaging effects of ionizing radiation
  • 2.8.2. Mechanisms of action of ionizing radiation on living organisms. General questions of pathogenesis
  • 2.8.3. Effect of ionizing radiation on cells
  • 2.8.4. The effect of ionizing radiation on the body
  • 2.9. Effect of space flight factors. Gravitational pathophysiology
  • Chapter 3 Cell Pathophysiology
  • 3.1. Types of damage and cell death. Universal cell response to damage
  • 3.2. Mechanisms of damage to cell membrane structures
  • 3.2.1. Impairment of the barrier function of biological membranes
  • 3.2.2. Violation of the structural (matrix) properties of the lipid bilayer
  • 3.3. Changes in intracellular metabolism upon injury
  • 3.4. Disturbance of the structure and functions of intracellular organelles upon damage
  • 3.5. Damage to the cell's genetic apparatus
  • 3.6. Cell damage due to hypoxia
  • 3.7. “Vicious circle” of cellular pathology
  • Chapter 4 General reactions of the body to damage
  • 4.1. General adaptation syndrome
  • 4.1.1. History of the development of the doctrine of stress
  • 4.1.2. Definition of stress, its etiology and types
  • 4.1.3. “Selye’s triad” and stages of general adaptation syndrome
  • 4.1.4. Scheme of the pathogenesis of general adaptation syndrome
  • 4.1.5. The mechanism of positive (adaptogenic) and negative effects of stress hormones
  • 4.1.6. Mechanisms of stress damage and the development of “stress diseases”
  • 4.1.7. Systems for natural prevention of stress damage
  • 4.2. Acute phase reactions
  • 4.3. Shock
  • 4.4. Coma
  • Chapter 5 the role of heredity, constitution and age in pathology
  • 5.1. Heredity and pathology. Etiology and pathogenesis of hereditary diseases
  • 5.1.1. Variability of hereditary characteristics as the basis of pathology
  • 5.1.2. Mutations as an etiological factor of hereditary
  • 5.1.3. Phenomenology of gene expression
  • 5.1.4. Classification of hereditary pathology
  • 5.1.5. Etiology and pathogenesis of gene diseases
  • 5.1.6. Etiology and pathogenesis of chromosomal diseases
  • 5.1.7. Genetic factors in the pathogenesis of multifactorial
  • 5.1.8. Genetic diseases of somatic cells
  • 5.1.9. Diseases with unconventional inheritance
  • 5.1.10. Methods for studying and diagnosing hereditary pathologies
  • 5.2. The role of the constitution in pathology
  • 5.2.1. Classification of constitution types
  • 5.2.2. Constitution types and diseases
  • 5.2.3. Factors influencing the formation of the type of constitution
  • 5.3. The importance of age in the occurrence and development of diseases
  • 5.3.1. Age and illness
  • 5.3.2. Aging
  • Chapter 6 reactivity and resistance of the body, their role in pathology
  • 6.1. Definition of the concept of “body reactivity”
  • 6.2. Types of reactivity
  • 6.2.1. Biological (species) reactivity
  • 6.2.2. Group reactivity
  • 6.2.3. Individual reactivity
  • 6.2.4. Physiological reactivity
  • 6.2.5. Pathological reactivity
  • 6.2.6. Nonspecific reactivity
  • 6.2.7. Specific reactivity
  • 6.3. Forms of reactivity
  • 6.4. Reactivity and resistance
  • 6.5. Factors determining reactivity
  • 6.5.1. The role of external factors
  • 6.5.2. Role of the constitution (see Section 5.2)
  • 6.5.3. The role of heredity
  • 6.5.4. Age value (see Section 5.3)
  • 6.6. Basic mechanisms of reactivity (resistance) of the body
  • 6.6.1. Functional mobility and excitability of the nervous system in the mechanisms of reactivity
  • 6.6.2. Endocrine system function and reactivity
  • 6.6.3. Immune system function and reactivity
  • 6.6.4. Function of connective tissue elements and reactivity
  • 6.6.5. Metabolism and reactivity
  • Part II typical pathological processes chapter 7 pathophysiology of immunity
  • 7.1. Functional organization of the immune system
  • 7.1.1. Basic Concepts
  • 7.1.2. Immune system cells
  • 7.1.3. Immune system molecules
  • 7.2. Immune response
  • 7.2.1. Stages of the immune response
  • 2. Humoral immune response (b-cell).
  • 7.2.2. Regulation of the immune response
  • 7.3. Immunodeficiency conditions
  • 7.4. Hypersensitivity reactions
  • 7.5. Graft rejection
  • Chapter 8 allergies. Autoimmune disorders
  • 8.1. Allergy
  • 8.1.1. Mechanisms of transition of a protective immune reaction into an allergic (damage reaction)
  • 8.1.2. Criteria for an allergic condition
  • 8.1.3. Etiology of allergic reactions and diseases
  • 8.1.4. Classification of allergic reactions
  • 8.1.5. General pathogenesis of allergic reactions
  • III. Stage of clinical manifestations (pathophysiological).
  • 8.1.6. Allergic reactions developing according to type I hypersensitivity
  • 8.1.7. Allergic reactions developing according to type II (cytotoxic) hypersensitivity
  • 8.1.8. Allergic reactions developing according to type III (immune complex) hypersensitivity
  • 8.1.9. Allergic reactions developing according to type IV (t-cell-mediated) hypersensitivity
  • 8.2. Pseudoallergic reactions
  • 8.3. Autoimmune disorders
  • Chapter 9 pathophysiology of peripheral (organ) circulation and microcirculation
  • 9.1. Arterial hyperemia
  • 9.1.1. Causes and mechanism of arterial hyperemia
  • 9.1.2. Types of arterial hyperemia
  • 9.1.3. Microcirculation during arterial hyperemia
  • 9.1.4. Symptoms of arterial hyperemia
  • 9.1.5. The meaning of arterial hyperemia
  • 9.2. Ischemia
  • 9.2.1. Causes of ischemia
  • 9.2.2. Microcirculation during ischemia
  • 9.2.3. Symptoms of ischemia
  • 9.2.4. Compensation for impaired blood flow during ischemia
  • 9.2.5. Changes in tissues during ischemia
  • 9.3. Venous stagnation of blood (venous hyperemia)
  • 9.3.1. Causes of venous stagnation of blood
  • 9.3.2. Microcirculation in the area of ​​venous blood stagnation
  • 9.3.3. Symptoms of venous stagnation of blood
  • 9.4. Stasis in microvessels
  • 9.4.1. Types of stasis and reasons for their development
  • 9.4.2. Disturbances in the rheological properties of blood, causing stasis in microvessels
  • 9.4.3. Consequences of blood stasis in microvessels
  • 9.5. Pathophysiology of cerebral circulation
  • 9.5.1. Disturbances and compensation of cerebral circulation in arterial hyper- and hypotension
  • 9.5.2. Disturbances and compensation of cerebral circulation in venous stagnation of blood
  • 9.5.3. Cerebral ischemia and its compensation
  • 9.5.4. Microcirculation disorders caused by changes in the rheological properties of blood
  • 9.5.5. Arterial hyperemia in the brain
  • 9.5.6. Brain swelling
  • 9.5.7. Brain hemorrhages
  • Chapter 10 inflammation
  • 10.1. Basic theories of inflammation
  • 10.2. Etiology of inflammation
  • 10.3. Experimental reproduction of inflammation
  • 10.4. Pathogenesis of inflammation
  • 10.4.1. The role of tissue damage in the development of inflammation
  • 10.4.2. Inflammatory mediators
  • 10.4.3. Disorders of blood circulation and microcirculation in inflamed tissue
  • 10.4.4. Exudation and exudates
  • 10.4.5. Release of leukocytes into inflamed tissue (leukocyte emigration)
  • 10.4.6. Regenerative processes in inflamed tissue
  • 10.5. Chronic inflammation
  • 10.6. General manifestations of inflammation
  • 10.7. The role of reactivity in inflammation
  • 10.8. Types of inflammation
  • 10.9. Course of inflammation
  • 10.10. Outcomes of inflammation
  • 6. Transition of acute inflammation to chronic.
  • 10.11. The importance of inflammation for the body
  • Chapter 11 fever
  • 11.1. Ontogenesis of fever
  • 11.2. Etiology and pathogenesis of fever
  • 11.3. Stages of fever
  • 11.4. Types of fever
  • 11.5. Metabolism during fever
  • 11.6. Function of organs and systems during fever
  • 11.7. Biological significance of fever
  • 11.8. Fever-like conditions
  • 11.9. The difference between fever and overheating
  • 11.10. Principles of antipyretic therapy
  • Chapter 12 Pathophysiology of Typical Metabolic Disorders
  • 12.1. Pathophysiology of energy and basal metabolism
  • 12.1.1. Energy metabolism disorders
  • 12.1.2. Basic metabolic disorders
  • 12.2. Starvation
  • 12.2.1. Fasting treatment
  • 12.2.2. Protein-calorie deficiency
  • 12.3. Pathophysiology of vitamin metabolism
  • 12.3.1. Fat-soluble vitamins Group A vitamins
  • 12.3.2. Water-soluble vitamins
  • 12.4. Pathophysiology of carbohydrate metabolism
  • 12.4.1. Disorders of carbohydrate metabolism at the stage of digestion (breakdown) and absorption
  • 12.4.2. Disorders of carbohydrate metabolism at the stage of glycogen deposition
  • 12.4.3. Disorders of intermediate carbohydrate metabolism
  • 12.4.4. Impaired renal glucose secretion
  • 12.4.5. Dysregulation of carbohydrate metabolism
  • 12.4.6. Disorders of carbohydrate metabolism
  • 12.4.7. Diabetes
  • 12.4.8. Metabolic complications of diabetes mellitus
  • 12.5. Pathophysiology of lipid metabolism
  • 12.5.1. Impaired digestion and absorption of lipids
  • 12.5.2. Lipid transport disorder
  • 12.5.3. Impaired transfer of lipids into tissues. Hyperlipemia
  • 12.5.4. Impaired fat storage
  • 12.5.5. Obesity and fatty liver
  • 12.5.6. Disorders of lipid and unsaturated fatty acid metabolism
  • 12.5.7. Phospholipid metabolism disorder
  • 12.5.8. Cholesterol metabolism disorder
  • 12.6. Pathophysiology of protein metabolism
  • 12.6.1. Impaired breakdown of food proteins and absorption of resulting amino acids
  • 12.6.2. Disruption of the processes of endogenous protein synthesis and breakdown
  • 12.6.3. Amino acid metabolism disorder
  • 12.6.4. Disturbance of the final stage of protein and amino acid metabolism
  • 12.6.5. Violation of the protein composition of blood plasma
  • 12.7. Pathophysiology of nucleic acid metabolism
  • 12.7.1. Disturbance of endogenous synthesis of DNA and RNA
  • 12.7.2. Disorders of the final stage of nucleic acid metabolism
  • 12.8. Disorders of water and electrolyte metabolism (dyshydria). Dehydration. Swelling
  • 12.8.1. Changes in the distribution and volume of water in the human body
  • 12.8.2. Loss and need for water in the human body in normal and pathological conditions
  • 12.8.3. Types of dehydration and reasons for their development
  • 12.8.4. The effect of dehydration on the body
  • 12.8.5. Water retention in the body
  • 12.8.6. Edema and dropsy
  • 12.8.7. Principles of therapy for water and electrolyte disorders
  • 12.9. Pathophysiology of mineral metabolism
  • 12.9.1. Disorders of macronutrient metabolism
  • 12.9.2. Disorders of micronutrient metabolism
  • 12.10. Acid-base disorders
  • 3. Partial pressure (tension) of oxygen in the blood (pO2)
  • 12.10.1. Gas acidosis
  • 12.10.2. Gas alkalosis
  • 12.10.3. Non-gas acidosis
  • 12.10.4. Non-gas alkalosis
  • 12.10.5. Combined acid-base disorders
  • Chapter 13 Pathophysiology of Tissue Growth
  • 13.1. Disorders of the main periods of human growth
  • 13.2. Hypo- and hyperbiotic processes
  • 13.2.1. Hypobiotic processes
  • 13.2.2. Hyperbiotic processes
  • 13.3. Tumor growth
  • 13.3.1. Epidemiology of tumor diseases in humans
  • 13.3.2. Tumors benign and malignant
  • 13.3.3. Etiology of tumors
  • 13.3.4. Biological features of tumors, mechanism of their development
  • 13.3.5. Pathogenesis of tumor growth (oncogenesis)
  • 13.3.6. Relationship between tumor and body
  • 13.4. Transplantation of cells, tissues and organs
  • Colored insert
  • 12.8.2. Loss and need for water in the human body in normal and pathological conditions

    A person must consume such an amount of fluid per day that is able to compensate for daily losses through the kidneys and extrarenal routes. The optimal daily diuresis for a healthy adult is 1200-1700 ml (in pathological conditions it can increase to 20-30 l and decrease to 50-100 ml per day). The removal of water also occurs through evaporation from the surface of the alveoli and skin - imperceptible sweating (from lat. perspiration insensibilis). Under normal temperature conditions and air humidity, an adult loses from 800 to 1000 ml of water per day in this way. These losses under certain conditions can increase to 10-14 liters. Finally, a small part of the fluid (100-250 ml/day) is lost through the gastrointestinal tract. However, daily fluid loss through the gastrointestinal tract in pathology can reach 5 liters. This occurs with severe disorders of the digestive system. Thus, daily fluid loss in healthy adults during moderate exercise

    Water loss

    Adult weighing 70 kg

    Child weighing up to 10 kg

    Water inflow

    Adult weight

    70 kg

    Child weighing up to 10 kg

    Drinking water

    When breathing and sweating

    Endogenous water*

    Requirement per 1 kg of weight

    1550-2950 30-50

    400-850 120-150

    * Endogenous (metabolic) water, formed in the process of metabolism and utilization of proteins, fats and carbohydrates, makes up 8-10% of the body's daily water requirement (120-250 ml). This volume can increase 2-3 times in some pathological processes (severe injury, infection, fever, etc.)

    Under various circumstances and situations in which a person may find himself, and especially in pathological conditions, daily losses and water consumption may differ significantly from the normal average. This leads to an imbalance in water metabolism and is accompanied by the development negative or positive water balance.

    12.8.3. Types of dehydration and reasons for their development

    Dehydration (hypohydria, dehydration, exicosis) develops in cases where water loss exceeds its intake into the body. In this case, an absolute deficiency of total body water occurs, accompanied by the development of a negative water balance. This deficit may be due to a decrease in volume

    intracellular body water or with a decrease in the volume of extracellular body water, which in practice occurs most often, as well as due to a simultaneous decrease in the volumes of intracellular and extracellular body water. Types of dehydration:

    1. Dehydration caused by primary absolute water shortage(water depletion, “desiccation”). This type of dehydration develops either as a result of limited water intake, or as a result of excessive excretion of hypotonic or completely electrolyte-free fluid from the body with insufficient compensation for losses.

    2. Dehydration caused by a primary deficiency of mineral salts in organism. This type of dehydration develops when the body loses and insufficiently replenishes reserves of mineral salts. All forms of this dehydration are characterized by a negative balance of extracellular electrolytes (primarily sodium and chloride ions) and cannot be corrected by drinking pure water alone.

    When dehydration develops, it is practically important to consider two things: the rate of fluid loss (if dehydration is caused by excess water loss) and how the fluid is lost. These factors largely determine the nature of developing dehydration and the principles of its treatment: with rapid (within several hours) loss of fluid (for example, with acute high small intestinal obstruction), the volume of the extracellular water sector of the body and the content of electrolytes that make up its composition first of all decrease ( primarily sodium ions). Lost fluid should be replaced quickly in these cases. The basis of transfused media should be isotonic saline solutions - in this case, isotonic sodium chloride solution with the addition of a small amount of proteins (albumin).

    Slowly (over several days) developing dehydration (for example, with a sharp decrease or complete cessation of water intake into the body) is accompanied by a decrease in diuresis and the loss of significant amounts of intracellular fluid and potassium ions. Compensation for such losses should be slow: over several days, fluids are administered, the main electrolyte component of which is potassium chloride (under the control of diuresis, which should be close to normal).

    Thus, depending on the rate of fluid loss by the body, acute and chronic dehydration. Depending on the predominant loss of water or electrolytes, hyperosmolar and hypoosmolar dehydration. With the loss of fluid with an equivalent amount of electrolytes, isosmolar dehydration.

    For correct therapeutic correction of various types of dehydration of the body, in addition to understanding the causes of dehydration, changes in the osmotic concentration of liquids and the volume of water spaces, due to which dehydration mainly occurs, it is necessary to know about changes in the pH of the body fluid. From this point of view, there is a distinction dehydration with a change in pH to the acidic side(for example, with chronic loss of intestinal contents, pancreatic juice or bile), to the alkaline side(for example, repeated vomiting with pyloric stenosis is accompanied by significant losses of HCl and potassium ions and a compensatory increase in the blood level of HCO 3 -, which leads to the development of alkalosis), and also dehydration without changing the pH of body fluids(for example, dehydration, which develops when the supply of water from the outside decreases).

    Dehydration due to a primary absolute lack of water (water depletion, “desiccation”). The development of dehydration due to a primary absolute lack of water can be caused by: 1) alimentary restriction of water intake; 2) excess water loss through the lungs, kidneys, skin (with sweat and through extensive burned and injured surfaces of the body). In all of these cases, hyperosmolar or isosmolar dehydration occurs.

    Restriction of water supply. In healthy people, restriction or complete cessation of the flow of water into the body occurs under emergency circumstances: among those lost in the desert, among those buried during landslides and earthquakes, during shipwrecks, etc. However, much more often, water deficiency is observed in various pathological conditions: 1) with difficulty swallowing (narrowing of the esophagus after poisoning with caustic alkalis, with tumors, esophageal atresia, etc.); 2) in seriously ill and weakened persons (comatose state, severe forms of exhaustion, etc.); 3) in premature and seriously ill children; 4) in some forms of brain diseases accompanied by a lack of thirst (idiocy, microcephaly), as well as in

    as a result of hemorrhage, ischemia, tumor growth, and concussion.

    With a complete cessation of the supply of nutrients and water (absolute starvation), a healthy person experiences a daily water deficit of 700 ml (Table 12-15).

    Table 12-15. Water balance of a healthy adult, ml, in a state of absolute fasting (according to Gamble)

    During fasting without water, the body begins to use primarily the mobile fluid of the extracellular water sector (plasma water, interstitial fluid), and later the mobile water reserves of the intracellular sector are used. An adult weighing 70 kg has up to 14 liters of mobile water reserves (with an average daily need of 2 liters), and a child weighing 7 kg has up to 1.4 liters (with an average daily need of 0.7 liters).

    The life expectancy of an adult with a complete cessation of the supply of water and nutrients (under normal environmental temperature conditions) is 6-8 days. The theoretically calculated life expectancy of a child weighing 7 kg under the same conditions is 2 times less. Children's bodies tolerate dehydration much harder than adults. Under the same conditions, infants lose 2-3 times more fluid per unit of body surface per 1 kg of mass through the skin and lungs. Water saving by the kidneys in infants is poorly expressed (the concentrating ability of the kidneys is low, while the ability to dilute urine is formed faster), and the functional water reserves (the ratio between the mobile water reserve and its daily requirement) in a child are 3.5 times less than in an adult. The intensity of metabolic processes in children is much higher. Consequently, the need for water (see Tables 12-15), as well as the sensitivity to its lack in children is significantly higher compared to an adult body.

    Excessive water loss from hyperventilation and increased sweating. In adults, daily water loss through the lungs and skin can increase to 10-14 liters (under normal conditions this amount does not exceed 1 liter). In childhood, especially large amounts of fluid can be lost through the lungs during the so-called hyperventilation syndrome, which often complicates infectious diseases. In this case, frequent deep breathing occurs, lasting for a considerable time, which leads to the loss of a large amount of pure (almost without electrolytes) water, gas alkalosis.

    During fever, a significant amount of hypotonic fluid can be lost through the skin (due to sweat with a slight salt content) and the respiratory tract. During artificial ventilation of the lungs, which is carried out without sufficient humidification of the respiratory mixture, there is also a loss of hypotonic fluid. As a result of this form of dehydration (when water losses exceed losses of electrolytes), the concentration of electrolytes in extracellular body fluids increases and their osmolarity increases - the sodium concentration in the blood plasma develops, for example, can reach 160 mmol/l (normal 135-145 mmol/l) or more . The hematocrit indicator increases, the content of blood plasma protein increases relatively (Fig. 12-43, 2). As a result of an increase in plasma osmolarity, water deficiency develops in cells, intracellular dehydration, which manifests itself as agitation and anxiety. A painful feeling of thirst appears, dry skin, tongue and mucous membranes appear, body temperature rises, and the functions of the cardiovascular system are seriously upset due to thickening of the blood, central nervous system, and kidneys. In severe cases, a life-threatening coma occurs.

    Excessive water loss through the kidneys. Dehydration from polyuria can occur, for example, with diabetes insipidus (insufficient production or release of ADH). Excessive loss of water through the kidneys occurs in the congenital form of polyuria (congenitally caused decrease in the sensitivity of the distal tubules and collecting ducts of the kidneys to ADH), some forms of chronic nephritis and pyelonephritis, etc. With diabetes insipidus, the daily amount of urine with low relative density in adults can reach 20 liters or more.

    Rice. 12-43. Changes in sodium content (Na, mmol/l), blood plasma protein (B, g/l) and hematocrit (Hct, %) with various types of dehydration: 1 - normal; 2 - hypertensive dehydration (water exhaustion); 3 - isotonic dehydration (acute loss of extracellular fluid with an equivalent amount of salts); 4 - hypotonic dehydration (chronic dehydration with loss of electrolytes)

    As a result, it develops hyperosmolar dehydration. If the loss of fluid is compensated, then water metabolism remains in balance, dehydration and disorders of the osmotic concentration of body fluids do not occur. If the loss of fluid is not compensated, then within a few hours severe dehydration develops with collapse and fever. A progressive disorder of the cardiovascular system occurs due to blood thickening.

    Loss of fluid from extensive burned and injured body surfaces. In this way, significant losses from the body of water with a low salt content are possible, i.e. loss of hypotonic fluid. In this case, water from the cells and blood plasma passes into the interstitial sector, increasing its volume (see Fig. 12-43, 4). At the same time, the content of electrolytes there may not change (see Fig. 12-43, 3) - it develops isosmolar dehydration. If the loss of water from the body occurs relatively slowly, but reaches significant proportions, then the content of electrolytes in the interstitial fluid may increase - developing hyperosmolar dehydration.

    Dehydration from lack of electrolytes. The development of dehydration from a lack of electrolytes can be caused by: 1) loss of predominantly electrolytes through the gastrointestinal tract, kidneys and skin; 2) insufficient supply of electrolytes to the body.

    The body's electrolytes have the ability to bind and retain water. Sodium, potassium and chlorine ions are especially active in this regard. Therefore, the loss and insufficient replenishment of electrolytes is accompanied by the development of dehydration. This type of dehydration continues to develop with the free intake of clean water and cannot be eliminated by the introduction of water alone without restoring the normal electrolyte composition of the body fluids. When electrolytes are lost, hypoosmolar or isosmolar dehydration may occur.

    Loss of electrolytes and water through the kidneys. A large amount of salts and water can be lost in some forms of nephritis, in Addison's disease (aldosterone deficiency), in polyuria with high osmotic density of urine (“osmotic” diuresis in diabetes mellitus), etc. (see Fig. 12-43, 4; Fig. 12-44). The loss of electrolytes in these cases exceeds the loss of water, and hypoosmolar dehydration.

    Loss of electrolytes and water through the skin. The electrolyte content of sweat is relatively low. The average concentration of sodium is 42 mmol/l, chlorine - 15 mmol/l. However, with profuse sweating (heavy physical activity, work in hot shops, long marches), their loss can reach significant values. The daily amount of sweat in an adult, depending on environmental temperature factors and muscle load, ranges from 800 ml to 10 l, while sodium can be lost more than 420 mmol/l, and chlorine - more than 150 mmol/l. Therefore, with profuse sweating without adequate intake of salt and water, dehydration is as severe and rapid as with severe gastroenteritis and uncontrollable vomiting. Developing hypoosmolar dehydration. Extracellular hypoosmia occurs and water enters the cells, followed by cellular edema. If you try to replace lost water with salt-free liquid, then intracellular edema worsens.

    Loss of electrolytes and water through the gastrointestinal tract. With chronic loss of fluid containing large amounts of electrolytes, hypoosmolar dehydration(cm.

    Rice. 12-44. Changes in the volume of intra- and extracellular fluid of the body, as well as shifts of water from one space to another under various pathological conditions in an adult: A - volume of intracellular fluid; B - volume of interstitial fluid; C - blood volume. Pl - blood plasma, Er - red blood cells

    rice. 12-43, 4). More often than others, such losses can occur through the gastrointestinal tract: repeated vomiting and diarrhea due to gastroenteritis, long-term non-healing fistulas of the stomach, pancreatic duct.

    With acute rapid loss of gastrointestinal juices (with pyloric stenosis, acute bacterial dysentery, cholera, ulcerative colitis, high small intestinal obstruction), changes in osmolarity and the composition of the extracellular fluid practically do not occur. In this case, salt deficiency occurs, complicated by the loss of an equivalent amount of fluid. An acute isosmolar dehydration(see Fig. 12-43, 3). Isoosmolar dehydration can also develop with extensive mechanical trauma, massive burns of the body surface, etc.

    With this type of dehydration (isosmolar dehydration), the loss of water by the body occurs mainly due to extracellular fluid (up to 90% of the volume of lost fluid), which has an extremely adverse effect on hemodynamics due to

    soon the onset of blood thickening. Figure 12-44 shows changes in the volume of intra- and extracellular fluid of the body, as well as the movement (shifts) of water from one water space to another during acute loss of extracellular fluid (see Figure 12-44,

    With rapid dehydration of the body, mainly interstitial fluid and blood plasma water are lost. In this case, there is a shift of water from the intracellular sector to the interstitial sector. With extensive burns and injuries, water from cells and blood plasma moves into the interstitial sector, increasing its volume. After severe blood loss, water quickly (from 750 to 1000 ml per day) moves from the interstitial water sector into the vessels, restoring the volume of circulating blood. With uncontrollable vomiting and diarrhea (gastroenteritis, toxicosis of pregnancy, etc.), the adult body can lose up to 15% of the total amount of sodium, up to 28% of the total amount of chlorine and up to 22% of the total extracellular fluid every day.

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