1 stage - compensation.

The body temperature is maintained at a normal level, although the ambient temperature is low, which is achieved by the restriction of heat transfer, activation of a sympathetic-adrenal system, which causes the spasm of the skin of the skin, thereby limiting the return of heat. At the same time there is an increase in heat product due to increased motor activity, reducing smooth muscles of the skin ("goose leather"), an increase in oxidative processes in the tissues.

2 Stage - Relative Compensation.

It develops at a very low ambient temperature or violation of the thermoregulation system. At this stage of the development of hypothermia, there is a combination of thermoregulation disorders and protective-adaptive reactions (strengthening oxidative processes in tissues). The heat transfer prevails over heat product, which causes a decrease in body temperature.

3 Stage - decompensation.

Hypoxia is developing due to the weakening of the external respiration, the oppression of cardiac activity, microcirculation disorders, there is a decrease in oxidative processes in the tissues. The patient becomes indifferent to the surrounding, immobilized, there is a strong physical weakness, bradycardia and a drop of blood pressure, rare superficial breathing. A person has a deep sleep. If he does not help, he will perish. In hypothermia, the need for an organism in oxygen decreases, the resistance to pathogenic effects increases, which is used in severe surgical operations (general and local hypothermia or "artificial hibernation").

Fever.

Fever - The overall response of the body for damage, the most important sign of which is to increase the temperature. This is a typical pathological process arising from the action of a pyrogen agent, which is based on an active restructuring of the functions of the center of heat regulation. Fever is one of the frequent manifestations of diseases, sometimes it can be the first and only symptom of the disease for a long time.

Etiology fever:

Fever is polyethylichic. For etiology, fever is divided into noncommunicable and infectious. There are a large number of noncommunicable diseases, accompanied by the development of fever. These include hemorrhages in the brain, traumatic damage to fabrics, burns, myocardial infarction and other organs, allergic diseases, etc. To infectious factors Below pathogenic viruses, microbes, fungi, simplest. Their components, vital products are called pyrogenins (from Greek. Pyros - fire, pyr - heat), which are divided into exogenous and endogenous.

Exogenous pyrogens Selected from microbial cells, they are an integral part of endotoxins. Some microbial exotoxins, such as diphtheria toxin, hemolytic streptococcal toxin have pyrogenic properties. The effect of exogenous pyrogenic substances is mediated through endogenous pyrogens, which are pylipeptides or proteins. The place of formation of endogenous pyrogen is all phagocytic cells (neutrophils, monocytes, macrophages, liver and spleen cells).

Hypothermia - The condition of the body, manifested by a decrease in body temperature below the norm, due to the effect of low ambient temperature and (or) a significant reduction in heat-product in it. The supercooling occurs when the heat transfer exceeds the heat product and the body loses heat. This occurs, with a significant decrease in the temperature of the environment of the environment, which is exacerbated by increasing air humidity, strong wind, as well as such factors as the lack of warm clothing and alcohol intake. The development of hypothermia is the process of stadium. In the development of hypothermia, three stages differ.

Compensation Stage Under conditions of exposure to low external temperature, it is characterized by an increase in heat product (reinforced muscle activity, intensification of metabolic processes) and a decrease in heat transfer (spasm of peripheral vessels, respiratory resignation, bradycardia). However, despite the low ambient temperature, the body temperature during this period is not reduced, and is maintained at the initial level due to the inclusion of compensatory reactions that determine the control of thermoregulation. Of the greater diversity of thermoregulatory devices, the mechanisms of physical thermoregulation are primarily included, aimed at limiting heat transfer. Under the conditions of cold production, the heat transfer is mainly limited due to the spasm of the vessels of the skin and decrease in sweating. With a more intense and prolonged action of the cold, the mechanisms of chemical thermoregulation are included, aimed at an increase in heat-product. Muscle tremor appears, the metabolism is enhanced, the decay of glycogen in the liver and muscles increases, the content of blood glucose increases. The consumption of oxygen increases, the systems ensure the delivery of oxygen to the tissues. The metabolism is not only rising, but also rebuilt. An additional output of energy in the form of heat is provided both by increasing the oxidative processes and due to the disagreement of oxidation and phosphorylation conjugate. In conditions of a long or intensive action of cold, overvoltage and depletion of thermoregulation mechanisms is possible, after which the body temperature decreases and the second stage of cooling is the stage of decompensation, or the actual hypothermia.

Stage decompensationit is characterized by breaking the mechanisms of regulation of thermal exchange (expanding the skin vessels, tachipne, tachycardia, etc.). The temperature homeostasis of the body is broken, as a result of which the homoothermal organism acquires the features of the pikeloterm. The basis of pathogenesis is a violation of the mechanisms of neuroendocrine regulation of metabolism and the functioning of tissues, organs and systems, the oppression of metabolic processes in the tissues. In this period, in addition to the reduction of body temperature, there is a decrease in metabolic processes and oxygen consumption; Vital functions are oppressed. Disruption of respiration and blood circulation leads to oxygen starvation, inhibition of the functions of the central nervous system, a decrease in immunological reactivity. In severe cases, irreversible changes in tissues leading to death are possible. In the second stage of hypothermia, the phenomena of the pathological and adaptive are closely intertwined. Moreover, the same shifts, being, on the one hand, pathological, on the other, can be assessed as adaptive. For example, the oppression of the functions of the CNS can be called the guard, since the sensitivity of nerve cells to the lack of oxygen and further decrease in body temperature is reduced. Reducing metabolism, in turn, reduces the need of an organism in oxygen.

It is extremely interesting that in a state of hypothermia, the body becomes less sensitive to the most diverse adverse effects of the external environment - a lack of oxygen and food, intoxication, infection, affecting the effect of electric current, ionizing radiation.

At the increase in the action of the cooling factor, a coma, freezing and death of the body develops.

Stage of coma, In the process of the occurrence of which the state of "cold anecia" is developing in a fall in blood pressure, breathing acquires the features of periodic, the level of metabolic processes is sharply reduced. Death usually occurs as a result of cessation of cardiac activity and paralysis of the respiratory center. The reason for the cessation of the contractile function of the heart is the development of fibrillation. The death of the body in hypothermia occurs, as a rule, when rectal temperatures are reduced below 25-20 ° C.

With a deep supercooling of the body, due to a sharp reduction in the level of metabolic processes, the need for tissues in oxygen is significantly discussed. This feature led to the creation of a method of artificial hypothermia, which is currently mandatory in the arsenal of surgeons and resuscitations. In surgical practice, it is sometimes necessary to operate on the "dry" heart, that is, free from blood (for example, under plastic operations about congenital defects), and sometimes several dozen minutes sometimes should be launched in the blood circulation. Application in this case, artificial hypothermia opens up great capabilities in cardiac surgery, allowing for a long time to operate under conditions of stopped blood circulation.

In surgical and resuscitation practice, it is also successfully applied local hypothermia headwith the help of a special helmet worn on the head, permeated with tubes, which circulates the coolant. This reduces the temperature of the brain and thereby increase the stability of nerve cells to hypoxia and at the same time leaves the body with free from cooling systems, which makes it easier to carry out surgical and resuscitation manipulations.

Artificial hypothermiait can be physical and chemical. Most often, these two types of hypothermia are used in combination.

Physical hypothermia is achieved by cooling the patient's body. When the apparatus of artificial blood circulation, blood circulating in it is cooled to 25-28 ° C.

Chemical hypothermia is caused by the administration of various chemicals and drugs affecting thermostat mechanisms and allowing the thermal balance of the body towards the heat loss. Combinedly applying the physical and chemical methods of hypothermia, it is possible to lower the body temperature to 16-18 ° C, significantly reduce the need of the brain in oxygen and sharply increase its resistance to hypoxia.

Controlled (artificial) hypothermia is used in medicine in two varieties: common and local.

Controlled hypothermia (medical hibernation) - Method of controlled decrease in body temperature or its part in order to reduce the intensity of metabolism, level of function of tissues, organs and their physiological systems, increase their resistance to hypoxia. In the conditions of artificial hibernation there is an increase in the stability and survival of cells and tissues. This makes it possible to turn off the organ of blood supply for several minutes with the subsequent restoration of its livelihoods and adequate functioning.

General controlled hypothermia (general artificial hibernation)used in operations on the so-called dry organs: the heart (eliminating the defects of its valves and walls), the brain and some others.

prof. K.M. Krylov
Common cooling, frostbite
(etiology, pathogenesis, clinic,
treatment)
St. Petersburg, 2014

"Biologically important that lower
Temperature border of life
Much wider than the top. 55 ° C.
somewhat higher insurmountable life
due to the coming
White coagulation, low temperatures
do not cause protein coagulation even with
Its freezing. "
"The more difficult organism, especially since he
Sensitive to low
Temperatures »
I.A. Thai, thermal lesions, 1938, 1966

1. Reverse dependence existing
between the degree of endurance of the body
in relation to the cold and complexity of it
Buildings.
2. To a large extent determining
The offensive of frostbite is
incomparably large resistance
fabrics, cells and generally live protein
Relation to cold than to heating.

Biological features of a cold injury

3. Slowing biochemical and
biological processes in chilled
plot coming after
Begins to deplete local
thermoregulation and falls fabric
temperature.
4. The hidden nature of damage in the period
hypothermia and manifest them later
a well-known deadline
Low temperature actions.
5. Contact fabric processes
(Timely help, correct treatment).

Cooling

General
Local

General cooling of the organism

Types of general hypothermia

1) Physiological
2) medical
3) Pathological
4) general cold injury

General cooling is a consequence of the impaired thermal balance and develops at:

Heat Pot.
Heat Production

Thermoregulation is a set of organism reactions aimed at maintaining physiological temperature.

Heat Production
Heat Pot.

With general cooling, phases differ:

A) compensation
Heat Pot.
Potting
Spasm vessels
B) decompensation
Heat Pot.
Heat Production
Heat Production
Metabolism
Heart rate, hell, mod
Glucose
Oxygen consumption in 5-6
time
5% oxygen consumption
Each degree decline
Temperature

MP Starks (1957), E.V. Maistrah (1962), G.A. Akimov et al. (1977)

General cooling - Impact
Cold, not accompanied
Reduced body temperature below 35 ° C.
Bulk overcooling - drop
body temperature below 35 ° C, when
Compensatory mechanisms of thermoregulation
do not cope with his destructive
Action
Freezing of the body - Pathological
hypothermia accompanied by dangerous
disorder of body functions up to
His death.
MP Starks (1957), E.V. Maistrah (1962), G.A. Akimov et al.
(1977)

For a person, a decrease in temperature in the rectum:

- before
about
25 S.
- very dangerous;
- up to 20 ° C - almost
irreversible;
-
about
17-18 S.
- Mortally.

Human body temperature in humans with different measurement methods Measurement method Norm rectal 36,6 ° C - 38.0 ° C OUT 35.8 ° C - 38.0 ° C frontal 35.8 ° C - 37.6

Body temperature rate in humans
Different methods of measurement
Method of measurement
Rectal
Oars
Frontal
Oral
Migratic
Norm
36.6 ° C - 38.0 ° C
35.8 ° C - 38.0 ° C
35.8 ° C - 37.6 ° C
35.5 ° C - 37.5 ° C
34.7 ° C - 37.3 ° C

Optimal place to measure
"Internal" body temperature is
tympanic temperature. Unlike
other areas of bodies that are usually
We use for measurement, value
Temperatures and local blood circulation in
Operations of the eardrum Maximum
approaches the value of blood temperature,
which feeds hypothalamus, center
Thermal regulation of the body.
New thermometers that measure through the hearing pass Radiation
Temperatures of the eardrum, the so-called "radiation locators,
infrared beam sensitive "or infrared thermometers
radiation (thii) with a temperature measurement range from 0 to 50 ○ s.

The severity of the state with general cooling depends:

Ambient temperature and
Duration of action
From meteorological factors
The state of thermal protection
From the strength and time of exposure
cold factor

The stability of the body is reduced at:

Physical treatment
Long starvation
Alcoholic intoxication
Blood loss
Shock
Injury
Age

Clinical Picture (Doreactive Period)

1) compensatory stage
2) Adamynova
3) Soporous
4) Comatosic

Compensatory stage

The victims are excited.
Complain about chills. Lubs
Cyanotic, skin
Pale, cold, symptom
"Goose skin", muscular trembling,
shortness of breath, tachycardia, increase hell,
Increase diuresis, temperature in
The rectum above 35 ° C.

Adamina Stage

Consciousness confused, inhibitable.
Headache complaints
dizziness, weakness, apathy,
drowsiness. Single of muscle tone,
inhibition of tendon reflexes.
Violation may be marked
Coordination of movements, violation
vision, hallucinations. Lung
Increased hell, heart tones
Muffled. Temperature in direct
The intestine above 35-30 ° C.

Soporant stage

A sharp depression of consciousness. Absence
Mimici, violation of speech, noted
Increase the skeletal tone
muscles. Skin pale,
Sometimes with a marble tint. Pupils
Expanded. Hell reduced, pulse from 50-30
Boots per minute. Breath
Surface. CHA 8-10 in 1 minute.
The temperature in the rectum 29-30 ° C.

Comatose stage

Consciousness is absent, pupils are expanded,
The corneal reflex is lost. Characteristic
Development of convulsive reduction and
Increase muscle tone. Rare breathing,
Surface up to 3-4 per minute. Pulse
Determined only on major arteries to
20 strikes per minute .ad reduced. Pronounced
Disorders of vital functions. Temperature
In the rectum below 25 ° C.

Reactive (postgotermic) period
After heating the body, the jet occurs.
As a rule, lethargy, fatigue, drowsiness,
Stiffness of movements, headache. At this time when
Silent overcooling can develop an internal edema
organs - brain, lungs, etc. is likely
The occurrence of thrombosis. Possible violations of cardiovascular activities, the development of acute renal
insufficiency, nervous disorders
Systems (asthenization, psychosis, trophic violations).
Subsequently, inflammatory
phenomena from the internal organs (pneumonia,
Bronchitis, plerites, jade, etc.). Forecast with heavy
The degree of general cooling is determined by evolving
complications.

Common cooling periods

I - compensatory
II - hypothermic
III - postgotermic
IV - Recovery
V - remote consequences

First period

compensatory, begins from the moment
exposure to low temperature up to
Began to reduce body temperature
below 36 ° C. Clinically muscular
shiver, feeling cold, apathy, lethargy,
Pallor skin with
Minor cyanosis. Breath,
Hell, pulse, diuresis - enlarged.

Second period

hypothermia since low
Temperatures below 36 ° C and up to 24 ° C
(termination of life or restoration of it
When assisting). Clinic - skin
covers from a pale cyanotic species to
Normal. Consciousness from stupor to
deep coma with vision disorder
The appearance of hallucinations. Defense
breathing and pulse gradually until full
Stop breathing, then pulse.
Slow decreased blood pressure, and when rendering
Aid is a gradual unstable

Third period

Nearest, postgotermic
(asthenic, encephalopathic),
Begins from the moment of recovery
Body temperature and counter
Temperature normalization (1-3 days).
Clinic - brain swelling, psyche violation
from hyperobability to coma,
Hyperthermia, increasing tendon
reflexes, memory violations,
non-uniform breathing, sharp

The fourth period

Recovery, starts from 2-3 days and
It lasts up to 2-3 months. Begins
with the standalization of body temperature
and ends with full or persistent
incomplete restoration of functions. Gone
gradual restoration of cardiovascular, pulmonary systems, psyche,
Neurological disorders disappear.
Restoration from the head of the gastrointestinal kidneys,
Immunological status.

Fifth period

Remote consequences. After reducing sharp
clinical manifestations from 2-3 months after
Injuries and can last for several years.
Clinically can manifest
Sensitivity to cold, asteration phenomena,
Violation of memory, speech, may be polyneurite,
hypercines, hyperhydrosis, neurodistrophic
Changes in the internal organs, in the bones,
joints, trophic disorders on the skin,
weight loss, reduce resistance to
infection

Emergency help

First aid. Transfer the victim B.
Warm room, cover clothes, give hot
Drink (tea, coffee). Common body massage.
Promotional help. Warming in the bathroom or
From any source of heat. Temperature in the bathroom
For 15-20 minutes, it should be raised from 30 to 40 ° C.
Massage. With the saved consciousness - inside
Hot tea, coffee.
Medical emergency care. In addition to
Activities of pretty aid -
intravenously 400 ml of warm 5% solution
glucose. Cardiac and respiratory
Analeptics do not enter!

Emergency help

In the medical institution with general
cooling II and III degree follows
Play the patient as quickly as possible in
Department of Anesthesiology and Resuscitation
(resuscitation and intensive therapy).
Intravenously (drip) - 400 ml of warm 5%
Glucose solution, 90-180 mg of prednisolone,
10 ml of a 5% solution of ascorbic acid (up to
3 times a day). Warming of the victim B.
Bathroom. Warming is carried out during
0.5-1.5 hours before rectal
temperatures up to 35 ° C. After heating, intravenous administration of 400 ml of 0.9% solution
NaCl, 400 ml of Reopolylukin, 100-150 ml of 4-
5% sodium bicarbonate solution.

Algorithm for medical care

Takes the victim doctor combustiologist. With violation of vital
Functions caused a anesthesiology physicreatologist.
When collecting anamnesis, find out
accompanying personnel
The duration of the exposure is cold
factor, condition of clothing and shoes,
The nature of assistance. In history
Mark air temperature.

It is necessary to make a thorough inspection
Patient, after removing all the clothes.
When examining the victims it is necessary
eliminate brain injury
internal organs, Oim, as it follows
keep in mind that more often overall cooling
It is a secondary diagnosis. If during
Surveys are detected
concomitant pathology, then in urgent
order to cause: therapist, neurosurgeon,
toxicologist, surgeon. The patient is heading
in the profile compartment with the recommendation
Plan treatment.

Measure the temperature B.
rectum and axillary
Wpadine, celebrate the pulse, hell,
Frequency and depth of breathing,
The state of pupils, muscular
Tone, character posture.

Survey of the patient urgently should
include:
1) blood on sugar
2) blood for residual nitrogen
3) blood for electrolytes (potassium, sodium)
4) blood on ethanol, to toxins.
5) Coagulogram.
6) Watering on ethanol, toxins.
7) Radioscopy of the chest organs.
8) Rengenography of skulls in 2 projections: an axial-axilar, side.
9) ECG and abdominal ultrasound ultrasound
10) Lumbal puncture (with no lack of
Contraindications: Heavy, Terminal State,
Hell is less than 90 mm.rt.st., signs of the suffering of temporal
Share of the brain and rear cranial pits)

With general cold injury in compensatory
Stages:
Only termination is required
cold.
1) the victim must be warm
Placing it in a room with a temperature
above 20 ° C or pack in a cotton blanket,
Warm sleeping bag. Give hot
Sweet drink. Wearing possible
Also blown in warm air,
Lighting the rains
Electroduct, light lamps,
Washing the stomach with warm water.

2) Medical Observation
It is necessary for 1-3 days.
3) in chronic diseases
Anamnesis must begin
Preventive treatment for
Warnings of exacerbation
diseases because cold
Injury contributes to exacerbation
Chronic diseases.

With general cold injury in
ADINAMIC STAGE:
Temperature of the body can
Normalize yourself.
1) intravenously enter the solution,
Heated to 40-45os
Containing: 30-50 ml. 40% rr
glucose, vitamin C 5% - 5.0 ml.,
Prednisolone 30-120 mg. for
reduction of hypoglycemia for
Reduction vascular
permeability and to reduce

2) general warming of the patient usually
It is carried out by immersing it in the bath with
water temperature approximately + 28 degrees.,
Gradually raising the temperature of the water to 3638 degrees. C. It is advisable to produce in the bath
Careful body rubbing soft
washbasins, which contributes to restoration
vascular tone and reflex
activity. Head and neck must be
Raised. It is important to follow the indicators
blood pressure. Active warming
Stop at a temperature in the rectum
33-34ºС to avoid development in subsequent
Hypertermic syndrome.

3) if the victim has
Local cold injury
limbs then on them
Thermal insulating are superimposed
Bandages and limbs in the bath is not
Immerse.
4) after heating in the bath
The victim is placed in
Department of intensive therapy for
Dynamic
Observations and infusion therapy.
All solutions are administered

5) B / in glucose is 10% - 400 ml. + Insulin
12 units. + Vitamin C 5% - 10 ml.
6) Polyglyukin 400 ml.
7) Intravenously sodium bicarbonate 4% 100-200 ml. To reduce acidosis.
8) intravenous solution containing:
200 ml of 10% glucose + 200 ml 0.25%
Novocaine + 15 ml - 300 mg of Trental + 5 ml
5% ascorbic acid. Enter
drip, heated to temperature
36-37 ° C (for improvement
microcirculation).

Introduction Cardiovascular
Tools
10) intravenously 10 ml 10%
Calcium chloride
11) into the subcutaneous tissue of the abdomen
Heparin 5000 units. 2 times a day with
daily reduction in dose in
For 5 days.
12) V / m 1 ml 1% Dimedrol
9)

With a coporous and comatose stage
When developing signs
respiratory failure
victim - trachea intubation and
Conducting IVL at the same time
Conducting the whole complex necessary
Therapy.
Warming of the chest area
Hearts, abdomen, liver area with
using electrollamps or heating

Glucose 40% - 40 ml, Vit. From 5% - 5.0
ml, prednisone 30-120 mg.
In / in glucose 5% - 400.0 + insulin 12
Units.
Vitamin C 5% - 10 ml
Polyglyukin 400.0
Sodium bicarbonate 4% - 200.0
Glucose 10% - 200.0 + Novocain 0.25%
- 200,0 +
Trental 300 mg - 5.0 +
Ascorbic K-5% - 5.0

Calcium chloride 10% - 10.0
Furosemid, Laziks 0.06g. or
Manitol 20% - 200.0
Contractor, Galds 100
Immunomodulators (styling,
polyoxidonium) 1.0 V / k - 5 days
Starting with 3 days
DIMEDROL 1% - 1.0
Heparin 5000 units. - 4 times / day
Corglikon 0.06% - 1.0
Antibiotics

V / m Lithic mixture: 2 ml 50%
Analgin, 2 ml 4% amidopyrin, 0.5 ml
2.5% aminazine and 1 ml. 2% of Dimedrol.
Enter h / s 3-4 hours after the start
warming with starting high
hypothermia
CA, PSS on perfectly
UHF for lower lumbar h / s 6-8 hours after
Beginning of warming
Soda inhalation
Mustard pieces, circular banks
Oxybarotherapy for the 2nd day after
Injuries

In the restorative period:
Physiosparces, respiratory
gymnastics
Vitaminotherapy
Tranquilizers. Bromids,
Tincture Ginseng, Eleteorocca
Aminalon, Gamalon 0,5g - 4
times / day
When violating speech - speech therapist • Emergency conditions in therapy • Precooling, stages of stroke, freezing

Precooling, stages of stroke, freezing

With a long stay in the cold due to the overall supercooling of the body, the celestation state may occur. His development contributes high humidity, strong wind, small mobility, fatigue, hunger, alcoholic intoxication.

When freezing, symptoms are marked:

• muscular tremor;
• initially, an increase in heart rate frequency, then its demolition and decrease in blood pressure;
• initially, the increase in breathing, then his immovation;
• the pallor of the skin with a blue tint, the skin is cold to the touch;
• decrease in body temperature;
• drowsiness;
• loss of consciousness;
• death.

The state of the victim, the symptoms and the necessary amount of emergency care depend on the stage (degree) of hypothermia.

1st stage - ADINAMIC. Her manifestations:

• injured intensive;
• speech is difficult, chant;

Stiffness of movements, muscular trembling;

a limited ability to independently move is preserved.

2nd stage - spooring. Her symptoms:

• the victim sharply injected, disoriented, often noncontected;
• pallor of skin, "marble" skin pattern;
• the pronounced stiffness of the muscles is characterized by the pose of the embryo;
• independent movements are impossible;
• decrease in blood pressure;
• breathing is rare, superficial.

3rd stage - convulsive or comatose. Her manifestations:

• lack of consciousness;
• the reaction of pupils into light is sharply weakened or lost;
• spastic reduction of chewing muscles;
• convulsions;
• defendment of heart rate;
• a sharp drop in blood pressure, often the pressure cannot be determined;
• breathing is rare, surface, pathological respiratory rhythms (irregular, intermittent, with pauses) are possible.

L. Savko

"Precooling, stages of staging, freezing" - article from the section

With violation of the thermal balance of the body, either hypertermic or hypothermal states are developing. Hyperthermic states are characterized by an increase, and hypothermic - decrease in body temperature above and below the norm, respectively.

Hypertermic states

Hypertermic states include the organism overheating (or actually hyperthermia), thermal impact, solar blow, fever, various hyperthermic reactions.

Actually Hypertermia

Hypertermia- a typical form of thermal exchange disorder, resulting in a result, as a rule, the actions of high ambient temperature and heat transfer disorders.

Ethiology causes hyperthermia

Allocate external and internal reasons.

High ambient temperature can affect the body:

♦ on hot summertime;

♦ in production conditions (at metallurgical and cast plants, with glass and stale);

♦ when eliminating fires;

♦ With long stay in a hot bath.

The decrease in heat transfer is a consequence:

♦ the primary disorder of the thermoregulation system (for example, when damaged by the respective hypothalamus structures);

♦ Disorders of the heat of heat into the environment (for example, fat people, with a decrease in the moisture permeability of clothing, high humidity).

Risk factors

♦ Impacts that increase the heat product (intensive muscular work).

♦ Age (hyperthermia develops easier in children and old men, which reduced the effectiveness of the thermoregulation system).

♦ Some diseases (hypertension, heart failure, endocrinopathy, hyperthyroidism, obesity, vegetative dystonia).

♦ Disadvantage of oxidation and phosphorylation processes in cell mitochondria through exogenous (2,4-dinitrophenol, dickurol, oligomycin, amital) and endogenous agents (excess thyroid hormones, catecholamines, progesterone, GWC and mitochondrial divisions - thermogenins).

Pathogenesis Hypertermia

Under the action of a hypertermic factor in the body, a triad of emergency adaptive mechanisms is included: 1) of the behavioral reaction ("care" from the action of the thermal factor); 2) the intensification of heat transfer and a decrease in heat-product; 3) stress. The deficiency of protective mechanisms is accompanied by overvoltage and disruption of the thermoregulation system with the formation of hyperthermia.

In the course of the development of hyperthermia, two main stages are distinguished: compensation (adaptation) and decompensation (dezadaption) of the mechanisms of thermoregulation of the body. Separate authors allocate the final stage of hyperthermia - hyperthermic to whom. Compensation Stageit is characterized by activation of emergency adaptation mechanisms for overheating. These mechanisms are aimed at increasing heat transfer and decrease in heat product. Due to this body temperature remains within the upper limit of the normal range. There is a feeling of heat, dizziness, noise in the ears, flickering "flies" and darkening in the eyes. May develop thermal neurasthenic syndrome,characterized by falling performance, lethargy, weakness and apathy, drowsiness, hypodynamines, sleep disorders, irritability, headaches.

Stage decompensation

The decompensation stage is characterized by the breakdown and inefficiency of both central and local thermoregulation mechanisms, which leads to a violation of the temperature homeostasis of the body. The temperature of the inner medium rises to 41-43 ° C, which is accompanied by changes in metabolism and functions of organs and their systems.

♦ Sweating decreasesit is often noted only a meager sticky sweat; The skin becomes dry and hot. Dry skin is considered an important feature of the decompensation of hyperthermia.

♦ Hydhiohydration increases.The body loses a large amount of liquid as a result of increased sweating and urica at the compensation stage, which leads to the organism hyphydrautation. Loss of 9-10% of the fluid is combined with essential vital disorders. This state is denoted as "Deserted Disease Syndrome.

♦ Hyperthermic cardiovascular syndrome develops:tachycardia is growing, cardiac emission is reduced, the IOC is maintained due to increased heart rate, systolic blood pressure can not grow long, and the diastolic blood pressure decreases; Microcirculation disorders are developing.

♦ Signs of exhaustion growmechanisms stressand the underlying adrenal and thyroid failure: hypodynamine, muscle weakness, a decrease in the contractile function of myocardium, the development of the hypotension, and up to the collapse are observed.

♦ Rheological properties of blood change:its viscosity increases, signs of sweet syndrome appear, disseminated intravascular coating of blood proteins (DVS syndrome) and fibrinolysis.

♦ Metabolic and physico-chemical disorders are developing:cl -, K +, Ca 2 +, Na +, Mg 2 + and other ions are lost; Water-soluble vitamins are derived from the body.

♦ Acidosis is recorded.Due to the increasing of acidosis, ventilation of lungs and the extraction of carbon dioxide increases; oxygen consumption increases; The dissociation of HBO 2 is reduced.

♦ Concentration increasesin the blood plasma so-called molecules of medium mass(from 500 to 5,000 yes) - oligosaccharides, polyamines, peptides, nucleotides, glyco- and nucleoproteins. These compounds have high cytotoxicity.

♦ The heat shock proteins appear.

♦ Significant modifiedphysical and chemical lipid state.Activated, the fluidity of membrane lipids increases, which disrupts the functional properties of membranes.

♦ in brain tissues, liver, lungs, muscles significantly increases the content of lipoperoxidation products- diene conjugates and lipid hydroperosis.

The well-being in this stage deteriorates sharply, growing weakness, heartbeat, pulsating headache, feeling of the strong heat and a feeling of thirst, mental arousal and motor anxiety, nausea and vomiting.

Hyperthermia may be accompanied by (especially with hyperthermic coma) by the enemy of the brain and its shells, the death of neurons, myocardial dystrophy, liver, kidney, venous hyperemia and phetechial hemorrhages in the brain, heart, kidneys and other organs. Some patients have significant neuropsychiatric disorders (nonsense, hallucinations).

With hyperthermic comastunning and loss of consciousness develops; Clonic and tetanic cramps, nystagm, the expansion of pupils can be observed, replacing them with narrowing.

Exodes

With the unfavorable flow of hyperthermia and the absence of medical care, victims die as a result of blood circulation deficiency, cessation of cardiac activity (ventricular fibrillation and ashistolia) and breathing.

Heatstroke

Heatstroke- acute form of hyperthermia with achieving hazardous body temperature values \u200b\u200bin 42-43 ° C (rectal) for a short time.

Etiology

High intensity heat action.

Low efficiency of body adaptation mechanisms to elevated external environment.

Pathogenesis

Heat strike - hyperthermia with a short compensation stage, quickly turning into decompensation stage. Temperature of the body tends to approach the temperature of the external environment. Mortality during thermal impact reaches 30%. The death of patients is the result of acute progressive intoxication, heart failure and stopping breathing.

Incixation of the bodymolecules of the average mass is accompanied by the hemolysis of erythrocytes, an increase in the permeability of the walls of the vessels, the development of the DVS syndrome.

Acute heart failureit is the result of acute dystrophic changes in myocardium, violation of actomyosine interaction and energy support of cardiomyocytes.

Stop breathingit may be a consequence of the growing hypoxia of the brain, the edema and hemorrhage into the brain.

Sunstroke

Sunstroke- Hypertermic state due to direct exposure to solar radiation energy to the body.

Etiology.The cause of the solar strike is excessive insolation. The greatest pathogenic effect is infrared of solar radiation, i.e. Radiation heat. The latter, in contrast to convection and conduction heat, simultaneously warms the surface and deep tissues of the body, including brain fabric.

Pathogenesis.The leading link of pathogenesis is the defeat of the CNS.

Originally develops arterial hyperemia of the brain. This leads to an increase in the formation of the intercellular fluid and to the compression of the substance of the brain. The compression of the skull of venous vessels and sinuses in the cavity contributes to the development of venous brain hyperemia. In turn, venous hyperemia leads to hypoxia, edema and small-scale hemorrhages in the brain. As a result, focal symptoms appear in the form of disorders of sensitivity, movement and vegetative functions.

The increasing disorders of metabolism, energy supply and plastic processes in the neurons of the brain will potentiate the decompensation of the mechanisms of thermoregulation, disorder of the functions of the CSS, respiration, gloomy of internal secretion, blood, other systems and organs.

The solar blow is fraught with a high probability of death (due to violation of the functions of the SSS and the respiratory system), as well as the development of paralysis, sensitivity disorders and nervous trophic.

Principles of therapy and prevention of hypertermic states

Treatment of victims are organized by taking into account the etiotropic, pathogenetic and symptomatic principles.

Etiotropic treatmentit is aimed at stopping the cause of hyperthermia and elimination of risk factors. For this purpose, methods aimed at normalizing heat transfer, cessation of high temperature and oxidative phosphorylation disabilities are used.

Pathogenetic therapyit intends to block the key mechanisms of hyperthermia and stimulation of adaptive processes (compensation, protection, recovery). These goals are achieved by:

Normalization of the functions of the CSS, respiration, volume and viscosity of the blood, mechanisms of neurohumoral regulation of the functions of sweat glands.

Eliminating the shifts of the most important parameters of homeostasis (pH, osmotic and oncotic pressure blood pressure).

Disinfecting the body (hemodilution and stimulation of the excretory function of the kidneys).

Symptomatic treatmentin hypertermic conditions, it is aimed at eliminating the unpleasant and painful sensations, aggravating the condition of the victim ("unbearable" headache, increased sensitivity of the skin and mucous membranes to heat, feelings of death and depression fear); Treatment of complications and related pathological processes.

Prevention of hypertermic statesdirected to prevent excessive impact on the organism of the heat factor.

Hypertermic reactions

Hypertermic reactionsit is manifested by a temporary increase in body temperature due to the transient predominance of heat-proof over heat transfer while maintaining thermoregulation mechanisms.

According to the criterion of origin, endogenous, exogenous and combined (malignant hyperthermia) are distinguished. Endogenous hyperthermic reactionsdivided into psychogenic, neurogenic and endocrine.

Psychogenic hyperthermic reactions are developing with strong stress and psychopathological conditions.

Neurogenic hypertermic reactions are divided into centrultural and reflex.

♦ Centrogenous hyperthermic reactions are developing with direct irritation of the neurons of the heat-regulation center responsible for heat-proof.

♦ Reflex hyperthermic reactions occur with strong irritation of various organs and tissues: the raging strokes of the liver and biliary tract; Lohanok kidneys and urinary tract when passing the concreters.

Endocrine hyperthermic reactions are developing as a result of the hyperproduction of catecholamines (under peuochromocytoma) or thyroid hormones (with hyperthyroid conditions). The leading mechanism is the activation of exothermic metabolic processes, including the formation of oxidation and phosphorylation disabilities.

Exogenous hyperthermic reactionsdivided into medicinal and immicking.

Medicinal (drug, pharmacological) hyperthermic reactions are due to LS that existent

effect: sympathomimetics (caffeine, ephedrine, dopamine), Ca 2 + - containing drugs.

Nelfarity hyperthermic reactions cause substances with a thermogenic effect: 2,4-dinitrophenol, cyanides, amital. These substances activate a sympathetic and thyroid system.

FEVER

Fever- a typical pathological process characterized by a temporary increase in body temperature due to the dynamic restructuring of the thermoregulation system under the action of pyrogen.

ETIOLOGY

The cause of fever - pyrogen. According to the source of the occurrence and the mechanism of action, primary and secondary pyrogens are isolated.

Primary pyrogens

Primary pyrogens themselves do not affect the thermoregulation center, but cause expression of genes encoding the synthesis of cytokines (pyrogenic leukokines).

By origin, infectious and noncommunicable primary pyrogens differ.

Pyrogens of infectious origin- The most frequent cause of fever. Lipopolysaccharides, lipotheaic acid, as well as exotoxins acting as spearntigen are assigned to infectious piezenms.

♦ Lipopolisaccharides(LPS, endotoxins) possess the greatest pyricity of LPSs is part of the microorganisms membranes, mainly gram-negative. Pyrogenic effect is typical of Lipid A, which is part of the LPS.

♦ Lipotheaic acid.Gram-positive microbes contain lipotheychic acid and peptidoglycans with pyrogenic property.

According to the structure of peyroins of non-infective genesis, proteins, fats, less often with nucleic acids or nucleoproteins. These substances can come from outside (parenteral administration to the body components of blood, vaccines, fat emulsions) or to form in the very organism (with noncommunicable inflammation, myocardial infarction, tumor decay, erythrocyte hemolysis, allergic reactions).

Secondary pyrogens.Under the influence of primary pyroges in leukocytes, cytokines (leucokines) are formed, having pyrogenic activity in a negligible dose. Pyrogenic leukokines called

secondary, true, or leukocyte pyrogenes. These substances directly affect the center of thermoregulation, changing its functional activity. Pyrogenic cytokines include il1 (previously designated as "endogenous pyrogen"), IL6, TNNα, γ-IFN.

Pathogenesis of fever

Fever is a dynamic and stadium process. According to the criterion for changing the body temperature, three stages of fever are distinguished: I.- temperature lifting, II.- standing temperature at elevated levels and III- Reducing the temperature to normal range.

Stage of temperature rise

Stage of body temperature lifting (stage I, sT. Incrementi)it is characterized by accumulation in the body of an additional amount of heat due to the predominance of heat-product over heat transfer.

Pyrogenic leukelocks from the blood penetrate through the blood hematciephalic barrier and in the precortic zone of the front hypothalamus interact with the receptors of nerve cells of the thermoregulation center. As a result, the membrane-bound phospholipase A 2 is activated and aghydonic acid is released.

In the neurons of the center of thermoregulation, the activity of cyclooxygenase significantly increases. The result of the metabolism of arachidonic acid over the cyclooxygenase path is to increase the concentration of PG 2.

Education PGA 2.- one of the key elevation links.

The argument of this is the fact of preventing fever when the activity of cyclooxygenase is suppressed by non-steroidal anti-inflammatory agents (NSAID, for example, acetylsalicylic acid or diclofenac).

PGA 2 activates adenylate cyclase, catalyzing education in the neurons of cyclic 3 ", 5" -Denozin monophosphate (CAMF). This, in turn, increases the activity of CAMF-dependent protein kinases, which leads to a decrease in the threshold of the excitability of cold receptors (that is, the increase in their sensitivity).

Due to this, the normal blood temperature is perceived as low: the impulses of the coolness of neurons in the address of the effector neurons of the rear hypothalamus increases significantly. In this regard, the so-called "Installation temperature point"the center of thermal regulation rises.

The changes described above are the central link of the mechanism for the development of stage I fever. They start the peripheral mechanisms of thermoregulation.

The heat transfer is reduced as a result of the activation of neurons of the nuclei of the sympathetic unit system located in the rear sections of the hypothalamus.

♦ The increase in sympathetic effects leads to a generalized narrowing of the lumen of the arteriole of the skin and subcutaneous fiber, reducing their blood flow, which significantly reduces the heat transfer.

♦ The decrease in skin temperature causes an increase in impulse from its cold receptors to the neurons of the thermoregulation center, as well as to the reticular formation.

Activation of heat-product (contractile and non-combustible thermogenesis).

♦ Activation of reticular formation structures stimulates processes of contractual muscular thermogenesisdue to the excitation of γ- and α-motoneurons of the spinal cord. The thermoregulatory ateonic state is developing - the tonic stress of skeletal muscles, which is accompanied by an increase in heat-product in the muscles.

♦ The growing effectant impulses of the rear hypothalamus neurons and the reticular formation of the stem portion of the brain determines the synchronization of the abbreviations of individual muscle beams of a skeletal muscles, which manifests itself as a muscular trembling.

♦ Non-worn (metabolic) thermogenesis- Another important mechanism of heat-product during fever. Causes of it: activation of sympathetic effects on metabolic processes and raising the level of thyroid hormones in the blood.

An increase in temperature is due to the simultaneous increase in heat-product and the limitation of heat transfer, although the significance of each of these components may be different. At stage I of fever, an increase in the main exchange increases the body temperature by 10-20%, and the rest is the result of a decrease in heat transfer by leather due to vasoconstrictions.

The temperature of the outer medium has a relatively small effect on the development of fever and the dynamics of body temperature. Consequently, with the development of fever, the thermoregulation system is not frustrated, and is dynamically rebuilt and works in a new functional level. This features fever from all other hyperthermic states.

Standing body temperature at elevated level

Stage of the body temperature at elevated level (stage II, sT. Fastigii)it is characterized by the relative balance of heat-product and heat transfer at a level substantially exceeding the validity.

Thermal Balanceinstalled due to the following mechanisms:

♦ increase the activity of thermal receptors of the precortic zone of the front hypothalamus caused by the increased blood temperature;

♦ The temperature activation of peripheral thermosensors of the internal organs helps to determine the balance between adrenergic influences and increasing cholinergic effects;

♦ The increase in heat transfer is achieved due to the expansion of the arterioles of the skin and subcutaneous fiber and strengthening;

♦ The decrease in heat product flows due to the decrease in the intensity of metabolism.

The combination of daily and stadium dynamics during fever is indicated as temperature curve.There are several typical varieties of the temperature curve.

♦ Constant.With it, the daily range of fluctuations in body temperature does not exceed 1 ° C. This type of curve is often detected in patients with equity pneumonia or abdominal typhoid.

♦ Remiterative.It is characterized by daily temperature fluctuations by more than 1 ° C, but without refund to the normal range (often observed in viral diseases).

♦ Abreasingor intermittent.The fluctuations of the body temperature during the day reach 1-2 ° C, and it can normalize for several hours, followed by its increase. This type of temperature curve is often registered in abscesses of lungs, liver, purulent infection, tuberculosis.

♦ Extinguishingor hectic.It is characterized by repeated increase in temperature during the day by more than 2-3 ° C with its rapid subsequent decrees. Such a picture is often observed during sepsis.

Some other types of temperature curves are distinguished. Considering that the temperature curve with infectious fever depends on the features of the microorganism, the definition of its type may be diagnostic.

During fever allocate several degrees of body temperature increase:

♦ weak, or subfebrile (in the range of 37-38 ° C);

♦ moderate, or febrile (38-39 ° C);

♦ high, or pyretic (39-41 ° C);

♦ Excessive, or hyperpirelicic (above 41 ° C).

The stage of reducing body temperature to normal

The stage of reducing the body temperature to the values \u200b\u200bof the normal range (stage III of the fever, sT. decrementi)it is characterized by a gradual decrease in leukokine products.

Cause:termination of primary pyrogen due to the destruction of microorganisms or noncommunicable pyrogenic substances.

Effects:the content of leukokins and their influence on the center of thermoregulation are reduced, as a result of which the "installation temperature point" decreases.

Varieties of temperature declineat stage III fever:

♦ gradual decline, or lithic(more often);

♦ rapid decline, or critical(less often).

Exchange of substances at fever

The development of fever is accompanied by a number of changes in metabolism.

BXat the I and II, the fever stages increase due to the activation of the sympathetic unit system, emissions into the blood of iodine-containing thyroid hormones and the temperature stimulation of metabolism. This provides energy and substrates of metabolism. Increased functioning of a number of organs and contributes to an increase in body temperature. At stage III fever, the main exchange is reduced.

Carbohydrate exchangeit is characterized by significant activation of glycogenolysis and glycolysis, but (due to the action of separators) is combined with low energy efficiency. This largely stimulates the collapse of lipids.

Exchange of fatsin the fever, it is characterized by the predominance of catabolic processes, especially with the protracted stage II. During the fever, the oxidation of lipids is blocked at the stages of intermediate products, mainly CT, which contributes to the development of acidosis. To prevent these disorders with long-term fevering conditions, patients should consume a large amount of carbohydrates.

Protein exchangewith a sharp moderate fever with an increase in temperature up to 39 ° C, it is not significantly upset. A long course of fever, especially with a significant increase in body temperature, leads to a violation of plastic processes, the development of dystrophy in various organs and the aggravation of the vital activity disorders in general.

Water-electrolyte exchangesusceptible to significant changes.

♦ At stage I, the loss of fluid is increasing in connection with an increase in the formation of sweat and urine, which is accompanied by the loss of Na +, Ca 2 +, Cl -.

♦ In step II, the emission of corticosteroids from adrenal glands (including aldosterone) and ADG in the pituitary gland is activated. These hormones activate the reabsorption of water and salts in the kidney channels.

♦ In stage III, the content of aldosterone and ADG decreases, the water and electrolyte balance is normalized.

Signs of renal, liver or heart failure, various endocrinopathies, malabsorption syndromes appear during fever with substantial defeat of the relevant authorities.

Functions of organs and their systems for fever

During the fever, the functions of organs and physiological systems are changed. The reasons:

♦ Impact on the body of the primary pyrogenic agent;

♦ fluctuations in body temperature;

♦ influence of body regulatory systems;

♦ Environmental involvement in the implementation of various thermostat reactions.

Consequently, this or that deviation of the functions of organs during a fever is their integrative reaction to the above factors.

Manifestations

Nervous system

♦ Non-specific neuropsychiatric disorders: irritability, poor sleep, drowsiness, headache; The confusion of consciousness, inhibition, sometimes - hallucinations.

♦ Increased skin sensitivity and mucous membranes.

♦ Violation of reflexes.

♦ Changes in pain sensitivity, neuropathy.

Endocrine system

♦ Activation of the hypothalamic-pituitary complex leads to increased synthesis of individual liberins, as well as ADG in the hypothalamus.

♦ Increasing ACTH and TG products in adenogipophyzé.

♦ Increased corticosteroid levels, catecholamines, T 3 and T 4, insulin.

♦ Changing the content of fabric (local) Bav - GHG, leukotrienes, kinines and others.

The cardiovascular system

♦ Tachycardia. The degree of increasing CCS is directly proportional to the increase in body temperature.

♦ often arrhythmias, hypertensive reactions, centralization of blood flow.

External breathing

♦ Typically, with an increase in body temperature, an increase in the volume of ventilation is light. The main stimulants of breathing are an increase in PCO 2 and a decrease in the pH in the blood.

♦ The frequency and depth of breathing varies in different ways: unidirectionally or multidirectional, i.e. An increase in breathing depth can be combined with a decrease in its frequency and vice versa.

Digestion

♦ Reducing appetite.

♦ Reducing salivation, secretory and motor functions (the result of the activation of the sympathetic unit system, intoxication and elevated body temperature).

♦ Suppression of the formation of digestive enzymes of the pancreas and yellow biscuits.

Kidney.Reveaning changes reflect only the restructuring of various regulatory mechanisms and functions of other organs and systems during fever.

Value of fever

Fever is an adaptive process, but under certain conditions may be accompanied by pathogenic effects.

Adaptive effects of fever

♦ Direct bacteriostatic and bactericidal effects: coagulation of alien proteins and reduce the activity of microbes.

♦ Indirect effects: the potentiation of specific and non-specific factors of the IBN system, the initiation of stress.

Pathogenic effects of fever

♦ The direct damaging effect of high temperature consists in coagulation of its own proteins, an impaired of electric generation, increasing the speed.

♦ Indirect damaging effect: functional overload of organs and their systems can lead to the development of pathological reactions.

Differences of fever from other hypertermic states

Hyperthermia is due to the high temperature of the outer medium, the heat transfer and heat production disorders, and the cause of fever - pyrogens.

In the overheating of the body, there is a violation of thermoregulation mechanisms, in hypertermic reactions - an inappropriate increase in heat-product, and during fever, the thermoregulation system is adaptively rebuilt.

When overheating, the body temperature rises passively, and with a fever - actively, with the costly significant amount of energy.

Principles and methods for the treatment of fever

It must be remembered that a moderate increase in body temperature during fever has an adaptive value consisting in the activation of a complex of protective, adaptive and compensatory reactions aimed at the destruction or weakening of pathogenic agents. Conducting antipyretic therapy is appropriate only when there is a damaging effect of hyperthermia on the livelihood of the body:

♦ with excessive (more than 38.5 ° C) increasing body temperature;

♦ in patients with decompensated MID or blood circulation deficiency;

♦ in newborns, breast-age and older children in connection with the imperfection of the body thermoregulation system.

Etiotropic treatmentdirected on the termination of the pyrogenic agent.

In case of infectious fever, antimicrobial therapy is carried out.

In the fever of non-infectious origin, measures take measures to stop entering the organism of pyrogenic substances (solid blood or plasma, vaccines, serums, protein-containing substances); removal from the body of the source of pyrogen agents (for example, necrotic tissue, tumor, the contents of the abscess).

Pathogenetic therapyit is intended to block key stones of pathogenesis and, as a result, a decrease in overly high body temperature. This is achieved:

Braking products, preventing or decreasing the effects of substances generated in the neurons of the center of thermoregulation under the influence of leukokinov: PGA, CAMF. For this purpose, cyclooxygenase inhibitors are used - acetylsalicylic acid and others

Blocade of synthesis and effects of leukocyte pyrogens (IL1, IL6, FNF, γ-IFN).

Reducing excess heat supply by suppressing the intensity of oxidative reactions. The latter can be achieved, for example, by using the preparations of Khains.

Symptomatic treatmentputs the task to eliminate painful and unpleasant sensations and states aggravating the patient's status. For

fevering to such symptoms include strong headache, nausea and vomiting, pain in the joints and muscles ("breaking"), heart arrhythmias.

Pyroterapy

Artificial hyperthermia (pyroterapy) in medicine is applied for a long time. Currently, therapeutic pyroterapy is used in combination with other impacts of drug and non-drugs. There are general and local pyroterapy. Total pyroterapy.General pyroterapy is carried out by reproducing the fever using purified pyrogens (for example, pyrogenal or substances that stimulate the synthesis of endogenous pyrogen). Moderate body temperature increase stimulates adaptive processes in the body:

♦ Specific and non-specific mechanisms of the IBN system (with some infectious processes - syphilis, gonorrhea, post-infectious arthritis);

♦ Plastic and reparative processes in bones, tissues and parenchymal organs (with their destruction, damage, dystrophy, after surgical interventions).

Local hyperthermia.Local hyperthermia per SE,as well as in the complex with other methods of treatment, reproduce to stimulate regional protection mechanisms (immune and nonimune), repair and blood circulation. Regional hyperthermia is induced in chronic inflammatory processes, erosions and skin ulcers, subcutaneous fiber, as well as during individual species of malignant neoplasms.

Hypothermal states

Hypothermal states are characterized by a decrease in body temperature below normal. The development of their development is the disorder of thermoregulation mechanisms, providing the optimal thermal regime of the body. There is a cooling of the organism (actually hypothermia) and controlled (artificial) hypothermia, or medical hibernation.

Hypothermia

Hypothermia- a typical form of thermal exchange disorder - arises as a result of the action on the body of a low temperature of the external environment and a significant reduction in heat-product. Hypothermia is characterized by a violation (broken) of heat-regulation mechanisms and is manifested by a decrease in body temperature below the norm.

ETIOLOGY

Causes of developmentcooling the body is diverse.

♦ Low external temperature - the most common cause of hypothermia. The development of hypothermia is possible not only with a negative (below 0 ° C), but also at a positive external temperature. It is shown that the decrease in body temperature (in the rectum) to 25 ° C is already dangerous for life; Up to 17-18 ° C - usually deadly.

♦ Extensive muscle parasites or a decrease in their mass (for example, with their hypotrophy or dystrophy).

♦ Violation of metabolism and reducing the efficiency of exothermic metabolic processes. Such states can develop with adrenal insufficiency leading to the deficiency in the body of catecholamines; with severe hypothyroid states; In injuries and dystrophic processes in the centers of the sympathetic nervous system.

♦ Extreme degree of body exhaustion.

Risk factorscooling the body.

♦ Increased air humidity.

♦ High speed air movement (strong wind).

♦ Increased humidity of clothing or its wetting.

♦ Cold water. Water is about 4 times more heat and 25 times more heat-conducting than air. In this regard, the freezing in water may occur at a relatively high temperature: at a water temperature of +15 ° C, a person retains a viability of no more than 6 hours, at +1 ° C - about 0.5 hours.

♦ long starvation, physical overwork, alcohol intoxication, as well as various diseases, injuries and extreme states.

Pathogenesis of hypothermia

The development of hypothermia is the process of stadium. It is based on its formation more or less long overvoltage and, in the end, the disruption of the mechanisms of thermoregulation of the body. In this regard, with hypothermia (as in Hypertermia), there are two stages of its development: compensation (adaptation) and decompensation (dezadaption).

Compensation Stage

The compensation step is characterized by activation of emergency adaptive reactions aimed at reducing heat transfer and an increase in heat-product.

♦ Changes in the behavior of an individual (directional departure from the cold room, the use of warm clothes, heaters, etc.).

♦ Reducing heat transfer (achieved due to a decrease and termination of sweating, narrowing the arterial vessels of the skin and subcutaneous tissues).

♦ Activation of heat products (due to an increase in blood flow in internal organs and an increase in muscle contractile thermogenesis).

♦ Inclusion of the stress reaction (the excited state of the victim, an increase in the electrical activity of the thermoregulation centers, an increase in the secretion of liberins in the neurons of the hypothalamus, in the adenocytes of the pituitary gland - ACTH and TSH, in the brainstant of the adrenal glands - catecholamines, and in their corticosteroids, in thyroid gland - thyroid hormones ).

Thanks to the set of specified changes, the body temperature although decreases, but does not go beyond the framework of the lower limit of the norm. If the causal factor continues to operate, then compensatory reactions can be insufficient. At the same time, the temperature is reduced not only by the coating fabrics, but also internal organs, including the brain. The latter leads to the disorders of the central mechanisms of thermoregulation, the discordination and inefficiency of heat-product processes - their decompensation is developing.

Stage decompensation

The decompensation stage (dezadaption) is the result of a breakdown of the central mechanisms of thermoregulation. At the stage of decompensation, the body temperature drops below the normal level (in the rectum it decreases to 35 ° C and below). Temperature homeostasis of the body is broken: the body becomes caught. Call circles are often formed, potentifying the development of hypothermia and disorders of the organism.

Metabolic vicious circle.Reducing the temperature of the tissues in combination with hypoxia inhibits the flow of metabolic reactions. The suppression of the intensity of metabolism is accompanied by a decrease in the release of free energy as heat. As a result, the body temperature decreases even more, which additionally suppresses the intensity of metabolism, etc.

Vascular vicious circle.The growing decrease in the temperature of the body during cooling is accompanied by the expansion of the arterial vessels (according to the neuro-paralytic mechanism) of the skin, mucous membranes, subcutaneous tissue. The expansion of the blood vessels and the influx of warm blood from organs and tissues accelerates the process of the body of heat. As a result, the body temperature decreases even more, the vessels are even more expanding, etc.

Nervous muscular vicious circle.The progressive hypothermia determines the decline in the excitability of nerve centers, including controlling the tone and muscle contraction. As a result, such a powerful heat-product mechanism is turned off as muscular contracting thermogenesis. As a result, the body temperature is intensively decreased, which further suppresses neuromuscular excitability, etc.

The deepening of hypothermia causes the braking of functions at the beginning of the cortical, and in the subsequent and subcortex nerve centers. Hydodymna, apathy and drowsiness, which can be completed by a room developing. In this regard, it is often distinguished by a step of hypothermic "sleep" or coma.

At the increase in the action of the cooling factor comes the freezing and death of the body.

Principles of treatment of hypothermia

Treatment of hypothermia depends on the degree of decrease in body temperature and the severity of the vital activity disorders. Compensation Stage.At the compensation stage, victims need mainly in the cessation of external cooling and warming the body (in a warm bath, heating, dry warm clothes, warm drink).

Stage decompensation

At the stage of decompensation of hypothermia it is necessary to conduct intensive comprehensive medical care. It is based on three principles: etiotropic, pathogenetic and symptomatic.

Etiotropic treatmentincludes the following activities.

♦ Measures to terminate the cooling factor and warming the body. Active heating of the body is stopped at a temperature in the rectum 33-34 ° C in order to avoid the development of the hypertermic state. The latter is likely because the affected function has not yet been restored by the adequate function of the body heat regulation system.

♦ Warming of internal organs and tissues (through the rectum, stomach, light) gives a greater effect.

Pathogenetic treatment.

♦ Restoration of effective blood circulation and breathing. If the respiratory is impaired, it is necessary to release the respiratory tract (from the mucus, reversible language) and carry out an air to air or gas mixtures with an increased oxygen content. If the activity of the heart is broken, then they perform its indirect massage, and if necessary, defibrillation.

♦ Correction of the KSR, the balance of ions and liquids. For this purpose, balanced salt and buffer solutions are used (for example, sodium bicarbonate), dextran colloidal solutions.

♦ Elimination of glucose deficiency in the body reach the introduction of its solutions of different concentrations in combination with insulin, as well as vitamins.

♦ When blood loss, blood, plasma and plasma substitutes are transfused. Symptomatic treatmentaims to eliminate changes

in the body exacerbating the condition of the victim.

♦ Apply funds to prevent brain, lungs and other organs.

♦ Eliminate the arterial hypotension.

♦ Normalize diuresis.

♦ eliminate strong headache.

♦ If there are frosthe farms, complications and concomitant diseases, they are treated.

Principles of hypothermia prevention

The cooling prevention of the body includes a set of events.

♦ Using dry warm clothes and shoes.

♦ Proper organization of labor and recreation during the cold season.

♦ Organization of heating points, providing hot power.

♦ Medical monitoring of participants in winter hostilities, exercises, sports competitions.

♦ Prohibition of alcohol reception in front of a long stay in the cold.

♦ Hardening the body and acclimatization of a person to environmental conditions.

Medical hibernation

Controlled hypothermia(Medical hibernation) - a method of controlled decrease in body temperature or its part in order to reduce the intensity of metabolism and functional activity of tissues, organs and their systems, as well as increasing their resistance to hypoxia.

Controlled (artificial) hypothermia is used in medicine in two varieties: common and local.

General managed hypothermia

Application area.Performing surgical operations in a significant reduction or even temporary termination

regional blood circulation. This was the name of operations on the "dry" bodies: the heart, brain and some others. Benefits.A significant increase in the stability and survival of cells and tissues in hypoxia conditions at a reduced temperature. This makes it possible to turn off the organ of blood supply for several minutes with the subsequent restoration of its livelihoods and adequate functioning.

Temperature range.Usually use hypothermia with a decrease in the rectal temperature to 30-28 ° C. If necessary, long manipulations create a deeper hypothermium using an artificial circulation apparatus, muscle relaxants, metabolic inhibitors and other influences.

Local controlled hypothermia

The local controlled hypothermium of individual organs or tissues (brain, kidneys, stomach, liver, prostate gland, etc.) is used if necessary for operational interventions or other therapeutic manipulations on them: blood flow correction, plastic processes, metabolism, LS efficiency.