Traumatic shock is an acutely developing due to injury, a polypatogenetic pathological process, characterized by significant violations of the functions of life support systems, primarily blood circulation, against the background of the extreme voltage of regulatory (adaptation) mechanisms of the body. Traumatic shock is one of the manifestations of the acute period of traumatic disease.

Skock pathogenesis links

Distributed household expression "pain shock", "Death from pain shock". The true cause of the development of traumatic shock is the rapid loss of a large amount of blood or plasma. Moreover, this loss is not obliged to be in the form of an explicit (outer) or hidden (internal) bleeding - a shock state can cause massive plasma exudation through the burned surface of the skin during burns.

It is important for the development of traumatic shock there is not so much the absolute value of blood loss, how much the speed of blood loss. With a quick blood loss, the body has less time to adapt and adapt, and the development of shock is more likely. Therefore, the shock is more likely when the wounded of large arteries, for example, the femoral.

Strong pain, as well as neuropsychic stress, associated with the injury, undoubtedly play a role in the development of a shock condition (although they are not its main reason) and aggravate the severity of the shock.

Factors leading to the development of traumatic shock or aggravating it are also injuries with damage to particularly sensitive zones (crotch, neck) and vital important organs (for example, wound in the chest, fractures of the Ryube with a violation of the function of external respiration, the cranial and brain injury). In such cases, the severity of the shock is determined by the blood loss, the intensity of pain syndrome, the character of injury and the degree of safety of the function of vital organs.

Fast and massive blood or plasmotherly lead to a sharp decrease in the amount of circulating blood in the injury body. As a result, blood pressure is quickly and strongly and strongly falls, the supply of tissues with oxygen and nutrients deteriorates, tissue hypoxia develops. Due to the lack of oxygen tissues, toxic admissible metabolic products accumulate in them, metabolic acidosis develops, intoxication increases. Lack of glucose tissues and other nutrients leads to their transition to "self-sufficiency" - lipolysis (disintegration of fat) and protein catabolism increase.

The body, trying to cope with blood loss and stabilize the blood pressure, reacts with a release in the blood of various vessels (in particular, adrenaline, norepinerenaline, dopamine, cortisol) and spasm of peripheral vessels. This can temporarily stabilize blood pressure on a relatively "acceptable" level, but at the same time further worsens the situation with the supply of peripheral tissues with oxygen and nutrients. Accordingly, metabolic acidosis, intoxication of unsophisticated metabolic products, catabolic processes in tissues are even more enhanced. The centralization of blood circulation occurs - primarily the blood supply to the brain, the heart, lungs, while the skin, muscles, organs abdominal cavity Load blood. Halfasting blood kidney leads to a decrease in the glomerular filtration of urine and deterioration of the excretory function of the kidneys, up to complete anuria (lack of urine).

The spasm of peripheral vessels and an increase in blood intake as a reaction to bleeding contributes to the blockage of small spasped vessels (first of all capillaries) tiny blood clots - blood clots. The so-called "DVS-syndrome" is developing - disseminated intravascular coating syndrome. The blockage of small vessels further enhances problems with the blood supply to the peripheral tissues and, in particular, the kidneys. This leads to a further increase in metabolic acidosis and intoxication. It may develop the so-called "coagulopathy of consumption" - a violation of blood flowing due to the massive consumption of the resulting agents in the process of common intravascular coiling. In this case, pathological bleeding may develop or resume bleeding from injury, and further exacerbation of the shock.

Reducing the blood supply to the adrenal glands and their functions against the background of increasing the need for "shock" tissues in glucocorticoids leads to a paradoxical situation. Despite high level Cortisol in blood (emissions!), There is relative adrenal insufficiency. It is explained by the fact that "thrown" less than need to fabrics, and poorly blood-made adrenal glands are not physically able to give more cortisol.

Attempts to cope with pain by increasing the secretion of endorphins (endogenous analogs of opiates) lead to further fall arterial pressure, Development of inhibition, lethargy, anegia. The reaction to the decrease in blood pressure and the high level of catecholamines in the blood is tachycardia (rapid heartbeat). At the same time, due to insufficiency, the circulating blood volume is simultaneously reduced by cardiac output (impact volume of the heart) and there is a weak pulse filling (up to a filamentary or undetectable pulse on peripheral arteries).

The outcome of heavy shock without treatment is usually agony and death. In the case of a relatively straight or middle severity Shock In principle, self-healing is possible (at some stage, the further promotion of the shock may be suspended, and in the future the state is stabilized, the body adapts and recovery). But it is impossible to rely on it, since the development of a shock state of any extent in itself indicates a breakdown of adaptation, that the severity of injury exceeded the compensatory capabilities of this particular body.

Shock can be primary (early), which occurs immediately after injury and is a direct reaction to the injury. The secondary (late) shock occurs 4-24 hours after the injury and even later, often as a result of additional trauma of the victim (during transportation, cooling, resumed bleeding, having a limb to the harness, from coarse manipulations when rendering medical care and etc.). A frequent variety of secondary shock is a postoperative shock of the wounded. Under the influence of additional traumatization, there are also relapses of the shock in the affected, usually within 24-36 hours. Often shock develops after removing the harness from the limb.

(51) Procedure for the accident at the production of AOCH:

1. Do not panic

2. When "ATTENTION TO ALL!" Turn on TV / radio to obtain a reliable info.

3. Close the windows, turn off the electrical appliances and gas.

4. Wear rubber boots, raincoat.

5. Take with you the necessary things: documents needed warm things, three-day stock of non-helped food.

6. After notifying the neighbors, it is quickly (not to panic) to leave the zone of possible infection perpendicular to the wind direction at a distance of at least 1.5 km.

7. Use PPCs (gas mask, cotton-gauze bandage, moistened with 2-5% soda / in 2% R-RE lemonic acid (chlorine / ammonia).

8. If it is impossible to leave the zone of infection - close tightly and flick / plug all air ducts and cracks. Drink only boiled or bottled water, comply with personal hygiene rules.

(52) Epileptic status (series epileptic attacks) refers to life-degrading states. With it, severe respiratory disorders arise, cardiovascular activities, circulation and blood distribution by organs. At the heart of these changes lies convulsive syndrome. As the epileptic status continues, the patient deepens the coma, muscle hypotension increases (in the period between attacks), reflexes are oppressed. Patients with lots of seizures, and especially in epileptic status, need immediate hospitalization and intensive therapy.

1. Ensure the upper respiratory tract.

2. Ensure peripheral venous access.

3. Then make drug treatment aimed at eliminating seizures, normalization of cardiovascular activity and exchange. Effective anticipant therapy measures are: intravenous administration 2 ml of 0.5% Diazepam solution (Seduxena) in 20 ml of 40% glucose solution. The mixture is injected slowly for 3-4 minutes. If, after 10-15 minutes after the introduction of the specified solution, the convulsions are not stopped, the introduction should be repeated. In the absence of the effect, 70-80 ml of 1% sodium thiopental solution are introduced intravenously. When falling blood pressure, cardiac glycosides are shown.

4. Ensuring adequate oxygenation (or oxygen supply through nasal grains, or tracheal intubation at low saturation and the inefficiency of the introduction of anticonvulsants).

5. In signs of brain deployment (anisocorium, decerebral or decortic closure, Cushing syndrome -Bradicoia, arterial hypertension, the increase in respiratory disorders) is the translation of the patient to the IVL, the administration of a bolus of mannitol 20% -0.25-0.5 mg / kg for 15-20 minutes, at the same time 10 mg of 1% of the furosemide solution is introduced.

6. Transportation of the patient to the nearest therapeutic institution, which has the ability to hold an IVL.

(53) The burnless defeat is 4 degrees:

1. I degree - redness and skin edema, acute pain.

2. II degree - redness and skin of the skin with the formation of bubbles filled with yellowish liquid (due to the bundle or detecting the epidermis)

3. III degree - the appearance of bubbles with jelly-like contents, part of the bubbles is destroyed, the death of the epidermis and the dermis with the formation of a dark red or dark brown stamp. Differ IIIA and IIIIB degree - with a dermal layer of skin die partially, with B - completely

4. IV degree - leather and driving fabrics are completely affected (fiber, muscles, vessels, nerves and bones). Frequently observed charring.

Burns I, II, IIIA degrees belong to superficial, IIIB and IV - to deep. With superficial burns are affected by the upper layers of the skin, so they are healing when conservative treatment (without the use of skin plastics). For deep burns, the death of all layers of skin and deep tissues is characteristic. In the treatment of these burns, it is necessary to apply operational methods for rehabilitation of skin.

(54) Electrotramma - electric shock caused by deep functional changes to the central nervous system, respiratory and SCCs, often combined with local tissue damage.

The specific biological effect of the current consists in an exciting action on muscles and nerve elements, leading to long-term disorders in the work of the potassium-sodium cell pump, and, as a result, to pronounced neuromuscular disorders (up to the fibrillation of ventricles and instant death).

Visual signs of electric tram are the "current signs", located in the fields of entrance and exit electrical charge. At these points, maximum changes in tissues under the influence of electric current occur.

After the current termination, the symptoms from the CNS are prevalent. There is a general weakness, loss or clouding of consciousness. Signs of electricians are more often reminded by a clinical picture when concussing the brain. Arises headache And dizziness, the patient is sluggish, inhibited, indifferent to the surrounding. Less often, when electric crawled, excitement, redness of the skin and motor anxiety.

From side of cardio-vascular system It is observed at first an increase, and then decrease in blood pressure, pulse and arrhythmia. It is often revealed to expand the boundaries of the heart. In severe cases, fibrillation of ventricles is developing. Wet wipes appear in the lungs, on radiography chest Signs of emphysema are found. Cough is possible, in some cases (especially with the previously existing pulmonary pathology), signs of acute respiratory failure are noted.

With damage to lightningIn addition to lesion by a very high voltage, it may be accompanied by heavy burns up to charred, the victim also may also be leaving the shock wave and additionally obtain traumatic damage (in particular - skulls)

PP: It begins with stopping the effect of current on the affected - disconnection from the current-supporting item. Then it is necessary to assess the state and first of all, the preservation of respiratory F-AI and blood circulation, if necessary. Regardless of the extent, all victims are subject to hospitalization. Also impose a aseptic bandage to the scene of the burn (if available).

PVP: The victims in a state of sharp excitement should be given chloralhydrate in the enema.
To combat hypoxia, which develops in the first hours after lesion, oxygen therapy is used.
To reduce headaches, dehydration means are shown: 40% glucose solution or a 10% sodium chloride solution in an amount of 7-10 ml. With a thrust headache associated with elevated intracranial pressure, spinal puncture produce. The number of issued spinal fluid At first puncture should not exceed 5-7 ml, with a repeated 10-12 ml.
With functional disorders nervous system Assign sedatives.

(55) ixodic ticks

The first signs of the bite of a tick can manifest themselves after two or three hours: weakness, drowsiness, chills, lubrication in the joints, light-friendly.

Characteristic symptoms of diseases:

Tick-borne encephalitis : fever, general weakness, headache, dizziness, pain in eyeballs, pain in the muscles, bones, decline in appetite; With severe forms - disorders of consciousness, hemipreps, bulbar symptoms, motor disorders, cervical muscles paresis and upper limbs; In chronic flow - Kozhevnikovskaya epilepsy.

Borreliosis (Lyme Disease): In acute period - Migrating erythema at the site of the tick bite, an increase is possible lymph nodesClose to the place of bite and conjunctivitis. After a few weeks - Nearby card nerves, meningitis, radiculonurite, multiple erythematous rashes on the skin. When chronic - Arthralgia, changing xp. polyarthritis; Polynereropathy, spastic parapapape, ataxia, memory disorders and dementia.

PMP:remove the ticks, pass it into the laboratory for analysis, according to the results - the introduction of anti-monetic immunoglobulin of human / antibiotic treatment (semi-synthetic penicillins, amoxicillin-clavulanate, sulfonamides - ceftriaxone).

Adrenergic Mediator Syndrome: List characteristic symptoms; List drugs (substare) in overdoses and poisoning which is characterized by the development of the specified syndrome.

Symptoms:midship, hypertension, tachycardia or heart rate within the upper limit of the norm, dry mucous membranes; Pale wet skin, intestinal peristalsis reduced

Characteristic for the following substances: Means from a cold containing adrenomimetics (naphtizin); Eufillin; cocaine, amitripthallin in the early phase of action; Mao inhibitors (a number of antidepressants and anti-parkinsonic drugs - SELEGILIN, TRANYLCIPROMIN); thyroid hormones; synthetic amphetamines; Fencycledine (general anesthetic, "sullen"); Lizerginic derivatives

Sympatholic mediator syndrome: list the characteristic symptoms; List drugs (substare) in overdoses and poisoning which is characterized by the development of the specified syndrome.

Symptoms: myiosis, hypotension, bradycardia, inhibition of breathing, intestinal peristalsis reduced, muscle hypotension, pale leather, wet, cold

Preparations (substances): Cloofelin, b-blockers, Channel blockers, reserpine, opiates

Healing Bee, Bumblebee: List the characteristic symptoms and possible complications; Give a detailed characteristic of the full standard for the first and prefigure, as well as the first medical care.

Symptoms:sensibility of burning and pain, local tissue edema, redness and local body temperature, weakness, dizziness, headache, chills, nausea, vomiting, sometimes urticaria, lower back pain and heartbeat, heartbeat

Possible complications:supervision of the upper respiratory tract, systemic anaphylaxis: generalized urctronic rash, swelling of the face, itching the skin, dry cough, laryngo and bronchospasm, dyspepsia, shock, lung edema, coma.

First aid:

4) From the wound to remove the sting (better than tweezers)

5) Place of population to handle the antiseptic (process the wound with ammonia alcohol or water with soap). Put a person with a raised limb position, immobilization

6) for strong pain give an anesthetic drug

7) to the place of bite to attach a cold

8) give a drink antihistamine drug (suprastin)

9) Abundant drink

With systemic anaphylaxia phenomena A 0.1% solution of adrenaline is introduced in / in 0.1 ml / year of life (10 μg / kg), antihistamine preparations (1% diploma solution, suprastin 2% R-p 0.03-0.05 ml / kg or TAVEGIL 0.1 ml / year of life), glucocorticoids (prednisone 5 mg / kg or dexamethasone 0.5 mg / kg)

With the phenomena of bronchospasm - Broncholitics (100-200 mg of salbutamola, 20-80 μg of the IPratropium of bromide on inhalation, 10-40 drops of Berodural in the nebulizer).

AOKHV and sorting effects: to name the substances of this group; pathogenesis of damage by these poisons; List the characteristic syndromes and symptoms during the damage to the above substances; Give a detailed characteristic of protective measures and the full standard for the provision of first medical care.

This group includes s, which, with inhalation poisoning, cause lesions of respiratory organs and toxic eases of lungs with the development of acute hypoxia. The first world war was applied chlorine, phosgene, dithosgen. Currently - phosgene, dithosgen, chlorpicrin.

Pathogenesis: The toxic emission edema develops, which is based on an increase in the permeability of the alveolar and capillary walls as a result of damage to the surfactant system and the proteins of the alveolar and capillary membrane, which leads to the rising of the liquid part of blood and proteins in the alveoli

By severity:

· Easy - toxic damage to the mucous upper respiratory tract and keratoconjunctivitis (inhalation dose 0.05-0.5 mg x min / l)

· Middle severity - toxic bronchopneumonium (0.5-3 mg x min / l)

· Heavy - toxic eaters of lungs (3-10 mg x min / l)

Forms of lesion:

1) Lightning - a feeling of burning in the nature of the nose, in the nose and rotoglot. Nausea appears, pronounced general weakness, a strong dry cough, bradypuna increases, developing cyanosis of the skin and mucous membranes. Then the amazed loses consciousness, breathing ceases. After stopping the breath after 3-5 minutes, cardiac activity ceases

2) Slow out shape - by periods: the increase in pathological manifestations, relative stabilization, recovered. During the increase in the increase in pathological manifestations, the following phases are distinguished: reflex manifestations, imaginary well-being and clinical manifestations Eveley Lekyki

3) the phase of reflex manifestations - the smell, an unpleasant taste in the mouth, a slight irritation of the mucous membranes of the respiratory tract, conjunctiv. Cianosis appears, breathing slows down. The pulse is rapidly, hell rises somewhat. Possible nausea, vomiting, dizziness, general weakness

4) Phase of imaginary well-being (latent) - cyanosis, small shortness of breath. Amazed fussy, motion discoordinated, over lungs percussively box sound. Respiratory noises are weakened. Phase duration 4-6 hours.

5) The phase of clinical manifestations of the eighty edema - a stubborn, exhausting cough, breathing is hampered, shortness of breath and cyanosis grow sharply. The amazed is worried, looking for a convenient position for himself (more often on all fours with lowered head). T 38-39. Over light - box sound, points of dullness are noted, usually in the rear-lower departments, the creative and wet small-pushed wheels are listened here. The amount of them increases. The pulse is readily, cardiac tones become deaf, hell decreases. The striking fading is increasingly increasing the amount of fluid (up to 2.5 liters per day). Breathing becomes noisy, bubble. The amount of urine is sharply reduced.

In the absence of complications, the recovery period lasts 7-10 days.

Protective events:

1. Timely use of filtering gas

2. Protective clothing

During the phases of reflex manifestations and imaginary well-being (latent):

1. Inhalation under the mask of fiscaline gas mask (fly anesthetic) or anti-liquid

2. Hiding from the cold and warming the striking

3. Evacuation on a stretcher with a raised head end or in the sitting position (+ harnesses on the lower limbs)

4. Abundant Washing Eye Water, Nose and Otrot

5. Installing in a conjunctival bag of 2 drops of 0.5% R-RA Dicaina

6. GKS: Becklomethasone Dipropionate inhaled by all amazed: 1st day - 4 One-time inhalation of 0.125 mg at once, and then within 6 hours every 5 min 2 inhalation. Then 1-2 inhalation after 10-15 minutes. Until the fifth day, in the presence or absence of changes in the lungs, 1 inhalation is made; before bedtime - 6 times 4-5 inhalations with 15-minute intervals; After waking up - 5 inhalations. After the 5th day, in the presence of changes in the lungs 1, the inhalation is hourly until complete recovery, in the absence of pathological changes in the lungs - 1 inhalation every 3-4 hours.

Inhalation administration of GCS can be replaced by intravenous methipred: the first day - 1000 mg, the second - the third - 800 mg, the fourths - the fifth - 500-700 mg, from the sixth day the dose is reduced by 100 mg per day - up to 100 mg. Next, it is necessary to reduce the dose of 10 mg per day - up to 50 mg. After that, they transfer to the reception of the drug inside with a decrease in a dose of 4-6 mg per day. The final dose of 4 mg is accepted for a long time.

7. Diprazine (Pipolfen) - 2.5% - 2ml

8. Ascorbic acid 5% - up to 50 ml

9. Ca preparations (calcium gluconate 10% -10 ml)

10. Promedol 2% -2 ml in / m

With the development of toxic edema lungs:

1. Morphine 1%: 1-1.5 ml of 10-15 ml of saline

2. GKS locally and systemically

3. Droperidol 0.25% - 2 ml

4. According to the testimony - diazepam 0.5% - 2ml

5. 35% or 40% oxygen-air mixture moistened with pairs of foaming agents

6. Gangliplays: Pentamine 5% - 1 ml in 9 ml of physical. R-ra, in / in 3 ml

7. Furosemid 20-40 mg V / in

8. According to the testimony: anticoagulants, vasopressors (dopamine, norepinephrine)

9. Antibiotic therapy

60) AOCHS and SCDS (general toxic): to name the substances of this group; pathogenesis of damage by these poisons; List the characteristic syndromes and symptoms during the damage to the above substances; give a detailed description of protective measures and the full standard for the first medical assistance ( including antidote therapy).

Substances: Sinyl Acid and Hlorcian

Pathogenesis: These poisons are oppressed by those enzymes, which includes a trailer iron, and, above all, the fermenters of tissue respiration (cytochrome) and an enzyme that catalyzing the splitting of hydrogen peroxide is catalase. Oyad bind cytochroma oxidase and reduce tissue respiration. As a result, the cells do not receive the necessary energy. First of all, the CNS cells suffer - shortness of breath is developing, the blood pressure is reduced, the pulse changes, convulsions appear.

Oxygen accumulates in the blood, the amount of oxymemoglobin increases, which gives blood and tissue alway color.

Characteristic syndromes and symptoms:

Typical initial signs - bitterness and metal taste in the mouth, nausea, headache, shortness of breath, convulsions.

Death comes from the termination of myocardial activities.

Two clinical forms:

1. Apoplexic: striking cries, loses consciousness, falls; After short-term clonic-tonic muscle cramps relax, tendon reflexes disappear; can be marked by exophthalm; Pupils are expanding, they do not react to the light. Hell drops sharply. The pulse is rare, filamentoid. Pale skin. After several breaths, breathing stops. Death comes within 1-3 min

2. Tightening form:

a) Stage of initial manifestations: feeling of the smell of bitter almond, slight irritation of conjunctiva and mucous nasopharynacles, numbness of the oral mucosa, anxiety, weakness, dizziness, heart pain, feeling of reinforced heartbeat, skin and mucous scarves, breath deepends and moreThe pulse changes (slows down), hell increases, vomiting, disruption of coordination of movements

b) Stage of shortness: Symptoms are growing, pronounced general weakness, urges are raised for defecation, the body temperature decreases, breathing a full mouth is reduced, additional respiratory muscles, the pulse is rare, stress, hell is increased, heart tones are enhanced, pupils are expanded, deep reflexes are raised, walking shaky, depression of consciousness

(c) Frajd stage: oppression of consciousness to coma. Tonic-clonic convulsions Relaxing. Convulsive cuts of chewing muscles. Breath rapidly, deep. The pulse of the weak voltage is often arrhythmic. During cramps, leather and mucous cianotic.

d) Comatose stage: no, the skin is pale with a cyanotic tint, the temperature is reduced, the breathing is superficial, arrhythmical, the pulse of weak filling, blood pressure is low, the heart tones are weakened. Death due to stopping breathing.

The feature of chlorocian poisoning is irritation of the mucous upper respiratory tract - sneaky, cough, dysnae, tears.

Protective events and first aid:

1. Timely application of gas masks (brand B, B8, M) and protective clothing

2. Neutralization on the terrain is not produced, but the inner premises are neutralized by a mixture of steam and formalin

3. Salts of seeding acid are degassed with a mixture consisting of 2 parts of 10% of the r-ra of the vitriol and one part of 10% of the RC

4. Antidote therapy with damage to cyanides

Specific antidote of cyanides - methemoglobinomotors (nitrites) - antisian, amylnitrite, sodium nitrite; Serio-containing compounds, carbohydrates, cobalt connections

A. First aid:amylnitrite - liquid for inhalation use, ampoules of 0.5 ml, under a gas mask

B. Promotional (Feldsher) Help: Anticyan 20% rr in ampoules in 1 ml, in / m 3.5 mg / kg or V2.5 mg / kg in dilution in 10 ml of 40% glucose; Oxigeotherapy, according to the testimony - Cordiamine 1 ml in / m

C. First Medical Help: repeated administration Anticyan in / in 30 minutes, repeated / m Introduction after 1 hour. In the absence of antibian - V / in 10-15 ml of 2% sodium nitrite (2-5 ml / min) under the control of blood pressure. With a weakening of cardiac activity, anagettices are used (1 ml of Cordiamine V / m); sodium thiosulfate 20-30 ml of 30% r-ra in / in; Glucose 40 ml of 40% R-RR / B, Oxigenotherapy, Introduction of cytochrome C, group vitamins, according to testimony - anallets, pressor amenines

Question number 61.: OV and AOKHV neurosu-paralytic action: to name the substances of this group, the pathogenesis of the damage by these poisons, list the characteristic syndromes and symptoms during the damage to the above substances, give a detailed description of the protective measures and the full standard for the first prefiguration assistance (including antidote therapy).

Substances of this group : Tabun, Zaror, Zoman, VX.

Pathogenesis : Phosphorian poisoning substances are associated with synapse cholineserase. The phosphorylated cholinesterase enzyme loses its activity. The depression of cholinesterase leads to accumulation of acetylcholine, impaired synaptic transmission. Holinoreceptors occurs, the fows can have a direct cholinomimetic effect on the postsynaptic membrane, increase the sensitivity of the synapse to acetylcholine.

Clinical picture :

7. central action (anxiety, emotional lability, dizziness, tremor, clonic-tonic convulsions, violation of respiratory and vascular centers, depression of consciousness)

8. Musarin-like action (spasm of smooth muscles, hypersecretion of glands, hypotension, bradycardia)

9. nicotine-like action (muscle weakness, sluggish paresis and paralysis, tachycardia and hypertension)

Protective events : Using a filtering gas mask, protective clothing, partial sanitary treatment with a liquid from an individual anti-chemical package, a weak solution of alkali when it gets into the skin, when you get rinsed with water, when you hit the stomach to cause vomiting, make a probe stomach wash and give sorbents.

Antidote therapy :

6. Antidot P-10M is used in the threat of defeat or in the first minutes of intoxication. The drug contains a reversible cholinesterase inhibitor, central cholinoblocators and antioxidant, a tablet of 0.2 grams.

7. Athens in a syringe tube of 1 ml. The drug contains central M-and H-cholinolics, a fenamine.

8. Budayshim in a syringe tube of 1 ml. It consists of N- and M-cholinolitic. Introduced in \\ m.

9. Atropine sulfate 0.1% - M-cholinolitic. With light shapes in \\ m 1-2 ml, repeated injections are possible in 2 ml in \\ m with an interval of 30 minutes. When the arrangement of medium gravity: 2-4 ml in \\ m, after 10 minutes 2 ml is reused. With severe lesions: 4-6 ml in \\ B, re-2-4 ml in \\ m in 3-8 minutes.

10. Dipicamine 15% in 1 ml ampoules - Holinesterase reactivator. With a light degree of lesion: 1 ml in \\ m, after 1-2 hours, 1 ml is reused. With a medium degree: 1-2 ml in \\ m, after 1-2 hours again. With severe lesions: 450-600 mg in \\ c.

11. Oxigenotherapy and all measures to ensure the maintenance of respiratory tract and respiratory support are also important + anticonvulsant therapy + vasopressors + infusion therapy.

Question number 62.: Oh psychomimetic action (psychomimetics): to name the substances of this group, the pathogenesis of damage to these poisons, list the characteristic syndromes and symptoms during the damage to the above substances, give a detailed characteristics of protective measures and the full standard for the first medical care (including antidote therapy).

Substances of this group : BZ, Lizerginic Acid diethylamide (DLK), Buffyenin, Mescalin.

Pathogenesis :

· BZ.. The mechanism is due to the blockade of central muskarino-sensitive cholinoreceptors and a violation of the cholinergic transmission in the GM. BZ molecules form a durable complex with m-cholinoreceptors. Due to the long blockade of these receptors, the circulation of acetylcholine in synapses is disturbed, morphological damage to the synaptic apparatus is developing, this leads to the imbalance of neurotiator systems.

· DLK. It is noted the ability of this psychotoxicant to cause the excitation of serotoninergic, adrenergic and cholinergic systems. There is reason to believe that Lizergin psychosis is associated with a violation of a mediator synaptic equilibrium: due to damage to the serotonin-engineer system, adrenergic and cholinergic suffer.

Clinical picture :

7) BZ.. Lesions easy severity There are 1-5 hours: general inhibition, low-speed, low speech activity, drowsiness, mudry and accommodation violations are possible. Lesions middle severitythere are after 1-2 hours, there is an alternation of delirium syndromes and light stunning. Periods of consciousness are coincided with manifestations of psychomotor excitation. Illusions and hallucinations visual, subject. Periodically disturbed orientation in space. The pulse is rapidly, hell is increased. The damage to severe degree is formed after 20 minutes - one and a half hours. Characterized by a long and deep permanent of consciousness and sharp psychomotor arousal. Violated orientation in time and space. Speech contact is not possible, hallucinatory sider is expressed, different kinds hallucinations. Pronounced mydriasis and disorders of accommodation. Ataxia is rude, with drops. Disconference and dysarthria. Hell is increased, the pulse is rapidly. Tahipoic, urination delay and intestinal atony.

8) DLK. Dizziness, general weakness, nausea, tremor, blurred vision. Distortion of perception of forms and color, difficulty focusing at the facility. Various psyche disorders. Signs of intoxication appear in 20-60 minutes. Reach maximum development after 1-5 hours. Incixation lasts 8-12 hours.

Protective events : BZ. - Gas mask, CHO, amynostigmine 0.1% 2ml in / m, Galanamin 0.5% 2ml in / m. In the absence of effect, re-administration. Also, these drugs can be administered intravenously by a 5% glucose solution. With a pronounced psychomotor excitation: triftatazine 0.2% 2ml, haloperidol 0.5% 2 ml + with 5 mg with a single reception. 1% morphine 2ml, anaprilin 0.1% 1ml in / m. Prevention of patient overheating. DLK - timely putting on gas mask, chso, neuroleptics, symptomatic therapy.

Question №63.: Skin-disruptive effects: to name the substances of this group, the pathogenesis of damage to these poisons, list the characteristic syndromes and symptoms during the damage to the above substances, give a detailed characteristics of the protective measures and the full standard for the provision of first medical care (including antidote therapy).

Substances of this group : Strong Hyprit, Luzit.

Pathogenesis : iprit Provide both local and resorbative effect on the body. The first manifests itself in the development of necrotic inflammation of tissues at the site of entering and penetrating the body. The resorbative action is expressed in a complex symptom complex. Several leading mechanisms in the pathogenesis of ipitic lesions can be distinguished:

4) allergic - the protein complex is formed + the IPRIT, which is produced by antibodies, sensitization and allergic reaction;

5) Local action - alkylation of proteins, leading to the destruction of cells;

6) cytostatic action - as a result of RNA damage, cell division is violated;

7) a shock actuator - develops as a result of blocking a number of organism enzymes.

Lewisitebinds with enzymes containing sulfur, they participate in tissue breathing. The foci of necrosis is developing in places where Luzit falls with blood flow. Blood coagulation increases, which leads to thrombosis.

Clinical picture :

7. Iprit - skin lesions are divided into 3 periods (hidden, stage of erythema, vesiculous-bullous, ulcerative-necrotic, healing stage); eye lesions - catarrhal conjunctivitis, blefarospasm, keratoconiactivitis; Inhalation lesions (easy degree - dry, runny nose, voice hoarseness, catarrhal inflammation of mucous respiratory tract; middle degree - Hyprint tracheobronchitis, sternum pain, protracted bronchitis: severe degree - Hyphered pneumonia and necrotic damage to mucous); Oral lesions - pain in the area of \u200b\u200bstomach, salivation, nausea, vomiting, diarrhea; Resortal action - subfebrile temperature, temperature 38-40 degrees (2 weeks stay, then decreases rapidly), shock-like states.

8. Luzitis - local manifestations (formed bubbles that do not have trends to merge, tense, surrounded by a bright red wedge of hyperemia, deep necrotization of fabrics), inhalation lesions (catarrhal rinofaring, lung swelling, chemical burn, necrotic pneumonia), oral manifestations - education ulcers, louisitic intoxication.

Protective events : mustard gas - Using a filtering gas mask, protective clothing, partial sanitary treatment with a liquid from an individual anti-chemical package, or 10-15% of the aqueous-alcohol hydrochloride chlorine, 2% process the skin, bubbles open the sterile needle, the surface is processed by a disinfectant solution, inhaled by inhalation Fitizilin under a gas mask, cavity of nose and oralogotroke rinse 0.25% solution of chlorine, abundant stomach wash 2-4% aqueous solution of drinking soda, reception activated coal. Comprehensive treatment - in a 30% sodium thiosulfate solution 20-30 ml (repeat every 3-4 hours), for detoxification purposes, 4% sodium bicarbonate. When Iprit gets into the stomach to remove the poison, it is recommended to cause vomiting, to wash the stomach with water, or 0.02% solution of soda, then introduce an adsorbent (25 g of activated carbon in 100 ml of water) and salt laxative. To combat general poisoning phenomena, it is used: sodium thiosulfate in a 30% solution of 25-50 ml, administered intravenously in order to enhance the processes of neutralizing the iprite in the body, glucose in 40% solution of 20-40 ml intravenously, as a favorable effect on cardiovascular -sudial disorders, the respiratory function of the blood and the normalizing disturbing metabolism; Calcium chloride - 10% solution of intravenously 10 ml, as a means of weakening itching, local inflammatory reactions and reducing the phenomena of general intoxication; blood substitutes of the type of polyvinylpyrrolidone (250 ml), which have a noticeable disinfecting effect; antihistamine preparations, vascular means (Cordiamin, caffeine, ephedrine); if necessary - both hearty drugs (stanfantine, korglikon); Sodium bicarbonate in 2% solution of 500 ml intravenously to eliminate the acidotic shift. Lewisite - gas mask, protective clothing, 10-15% water-alcohol solution of chlorine (neutralization on the skin), 0.25% solution of chlorine for the eyes, when inserted into the stomach, washing with 2% solution of drinking soda, with inhaled damage the scene mixture. Unitiol - in \\ m or in \\ B at the rate of 1 ml by 10 kg, dicaptol 2.5-3 mg \\ kg V \u200b\u200b\\ m, Berlition - B \\ 300 mg in 250 ml of 0.9% NaCl.

Question number 64.: OV irritant (polycimators and sternites): to name the substances of this group, pathogenesis of damage to these poisons, list the characteristic syndromes and symptoms during the damage to the above substances, give a detailed description of the protective measures and the full standard for the provision of first medical care (including antidote therapy).

Substances of this group : Lacrimator, Stern, Si-Es, C-AR.

Pathogenesis : These substances affect the sensitive nerve endings of the mucous membranes of the upper respiratory tract and have an irritant effect on the mucous eye.

Clinical picture : feeling of tickness, soreness, burning in the nose and in the throat, head and dental pain, in the area of \u200b\u200bthe ears, rhinora, dry painful cough, salivation, nausea, vomiting, mucous membranes, edema, bradycardia, bradypognoe. In severe cases, sensitivity disorder, muscle weakness. The lesions of the polycimators are characterized by a sharp irritation of the conjunctions and cornea + the above symptoms. With the defeat of the SI-ES, an irritant effect on the skin + the above symptoms occurs.

Protective events : Filtering gas mask, skin protection, mouth rinsing and naked with water or 2% sodium bicarbonate, affected eyes are washed with water, in a conjuncting bag of 2 drops of 0.5% dicaine solution, non-nucleic analgesics, tranquilizers, ficilla inhalation to eliminate reflector disorders.

Question number 65.: Ammonia: The pathogenesis of the defeat of the AOCH data, list the characteristic symptoms and syndromes during the damage to the above substance, give a detailed characteristics of protective measures and the full standard for the provision of first medical care.

Clinical picture : When exposed to small ammonia concentrations, light phenomena of rhinitis, pharyngitis, tracheite, bronchitis are observed. The duration of poisoning is 3-5 days. When exposed to large concentrations noted coughing, pain and softening in the chest, diffuse mucous-purulent bronchitis. In some cases, at very large ammonia concentrations, the pulmonary spasm comes, pneumonia. With eye damage, there is a tearing, light-free, spasm of the eyelids, conjunctivitis, while entering liquid ammonia on the skin - burn with erythema, bubbles. Ammonia couples cause more often erythema.

Protective events :

9. The victim immediately should be taken out of the affected zone;

10. In case of impossibility of leaving the affected area, it is important to provide oxygen access;

11. The oral cavity, the throat and nose are washed with water for about 15 minutes (additional rinsing efficiency is ensured by adding lemon or glutamic acid into water);

12. Over the next day, after the defeat, absolute peace is ensured, which is important even with a slight degree of poisoning;

13. For eye, 0.5% Dicaine solution should be used, additionally, they can be closed with a bandage;

14. If the poison hit, it is necessary to rinse it as quickly as possible with water, then impose a bandage;

15. The ingress of poison in the stomach requires its washing.

Acute poisoning drug from the group of benzodiazepines: pathogenesis of the lesion; description of the clinical picture (characteristic symptoms); detailed feature assistance - first and prefigured; First medical (including measures to remove non-venerable poison and antidote therapy).

Pathogenesis

Understanding in the CNS is achieved by the stimulation of the GABC and receptors with increasing flow of chlorine ions. In addition, inactivation and reverse adenosine capture are suppressed, which leads to stimulation of adenosine receptors.

Clinic

The state of intoxication by sleeping equipment as a whole resembles alcohol intoxication, characteristic features are increasing inhibition, drowsiness, discoordination of movements. Affective sphere is characterized by emotional lability. The easiest degree of familiar intoxication will first be accompanied by an increase in mood. But at the same time, fun, a sense of sympathy for the interlocutor can easily move into anger, aggression towards others. Motor activity increases, but movements are messy, not coordinated. Sexual attraction can increase, appetite.

For intoxicating sleeping pills and sedatives Middle and heavy degrees of gravity are characterized by gross somatic and neurological violations. It is often hypersioned, hyperemia Scler. Skin covers become salon.

When increasing the degree of intoxication, a person falls asleep, sleep deep. Bradycardia, hypotension are marked. Pupils are expanded, the reaction of them to the light is sluggish, the nistagm, diplopia, dysarthria, the attraction of surface reflexes and muscle tone, ataxia is noted. May be observed involuntary defecation, urination. In severe intoxication, the oppression of consciousness increases, deep sleep goes to whom. Blood pressure drops sharply, the pulse is frequent, superficial. Breathing Shallow, frequent, with the deepening of the coma becomes rare, even more superficial, acquires frequency (Chen-Stokes breathing). The patient is sharply pale, the body temperature drops, deep reflexes disappear.

The prevention of shock did not find: (((

Shock(From English. Shock - Strike) - acutely developing syndrome, characterized by a sharp decrease in capillary (exchange, nutritional) blood flow in various organs, insufficient supply of oxygen, inadequate removal from the tissue of the exchange products and manifested by severe disorders of the body's functions.

Shock you need to distinguish from collapse(from Lat. Collabor - pay, to discharge), since sometimes the same condition denote as shock, then as a collapse, for example, a cardiogenic collapse, cardiogenic shock. This is due to the fact that in both cases there is a drop in blood pressure. Collapse is an acute vascular failure characterized by a sharp decrease in blood pressure, a decrease in the mass of circulating blood. A man is losing consciousness. The shock also reduces blood pressure and darkens consciousness.

However, between these two states there are fundamental differences. When the collapse, the process develops with primary failure of a vasoconstrictor reaction. When shock due to the activation of the sympatho-studary system, Vasoconstriction is sharply expressed. It is also the initial link of the development of disorders of microcirculation and metabolism in the tissues that received the name of the shock-specific, which are not under collapse. For example, with blood loss, hemorrhagic collapse can first develop, and then the transformation of the process in shock may occur. There are still some differences between collapse and shock. With shocks, especially traumatic, it is basically two stages in their development: excitation and oppression. In the excitation stage, blood pressure is even elevated. When Collapse, there is no stage of excitation and consciousness turns off completely. With shocks, the consciousness is confused and turns off only in the later stages and in severe cases of development.

Ethiology distinguish the following types of shocks: 1) hemorrhagic; 2) traumatic; 3) dehydration; 4) burn; 5) cardiogenic; 6) septic; 7) anaphylactic.

Naturally, the pathogenesis of each type of shock has its own features of development, its leading links. Depending on the nature of the current cause and characteristics of developing damage, the main leading pathogenetic links are becoming: hypovolemia(absolute or relative), painful irritation, infectious process at the stage of sepsis. Their ratio and severity with each form of shock are different. At the same time, the general links can be allocated in the mechanisms of development of all types of shock. It becomes a consistent inclusion of two types of compensatory-adaptive mechanisms.

First (Vasoconstrictor) Type - Activationsympathoadrenal and pituitary and adrenal systems. They are included in leading pathogenetic links. Hypovolemia is absolute (blood loss) or relative (reduction of the minute volume of blood and venous return to the heart) leads to a reduction in blood pressure and irritation of baroreceptors, which through the central nervous system activates the specified adaptive mechanism. Painful irritation, like sepsis, stimulates its inclusion. The result of the activation of sympathoadrenal and pituitary-adrenal systems is the emission of catecholamines and corticosteroids. Catecholamines cause a reduction in vessels that have pronounced α- adrenoreceptation:mainly skin, kidneys, abdominal organs. Nutritive blood flow in these organs is dramatically limited. Coronary and brain vessels do not have these adrenoreceptors, so do not decrease. This is the so-called "Circulatory Centralization",i.e., the preservation of blood flow in vital organs is the heart and brain and maintained pressure in large arterial vessels. This is precisely the biological significance of the inclusion of the first type of compensatory-adaptive mechanisms.

However, a sharp limitation of skin perfusion, kidneys, abdominal organs causes them to ischemia. Hypoxia arises. This includes second (vasodiletatory) typemechanisms aimed at eliminating ischemia. Vazoactive amines, polypeptides and other biologically active substances, causing the expansion of vessels, increase their permeability and violation of the rheological properties of blood begin to form. Significant contribution to their education is made by damaged tissues in which there is a decay of fat cells, activation of proteolytic systems, output from the cells of potassium ions, etc. The inadequacy of a vasodileater type of compensatory and adaptive mechanisms due to excess formation of VAZO develops active substances. All combined changes in the tissues, reducing the capillary and enhancement of shunt blood flow, changing the reaction of the prokapillary sphincters on catecholamines and increasing the permeability of capillary vessels. The rheological properties of blood change are changed, "vicious circles" are included. These are shock-specific changes in microcirculation and exchange. The result of these disorders is the yield of fluid from vessels in tissue and a decrease in venous return. The "vicious circle" is included at the level of the cardiovascular system, leading to a decrease in cardiac output and reduce blood pressure. The pain component leads to the oppression of the reflex self-regulation of the cardiovascular system, exacerbating developing disorders. The course of shock goes to the next, more severe stage. Disorders of the lung function arise ("Shock light"), kidneys, blood coagulation.

With each form of shock, the degree of activation of sympatho-studary and pituitary-adrenal systems, as well as character, the number and ratio of various types of formed biologically active substances are different, which is reflected on the speed and degree of development of microcirculatory disorders in various organs. The development of shock also depends on the state of the body. All factors causing its weakening (reconstruction period, partial fasting, hypocinezia, etc.) will contribute to the development of shock. Conversely, favorable working conditions, life, physical burden brakes its occurrence.

Hemorrhagic shock.It occurs with external (knife, bullet injury, arrosive bleeding from the stomach with ulcerative disease, tumors, from the pulmonary with tuberculosis, etc.) or internal (hemotorax, hemoperitoneum) bleeding in conditions of minimal tissue injury.

Traumatic shock.It occurs with severe injuries of organs, abdominal and chest cavities, a musculoskeletal system, accompanied by even minimal blood loss. Increasing blood loss in these cases takes the development of shock. It also distinguishes erectile and trapid stages. In the erectile stage there are speech and motor excitation, the pallor of the skin, tachycardia, a temporary increase in blood pressure. These signs are largely associated with the activation of the sympathoadrenal system.

The erectile stage goes to the torpedo. The clinical picture of this stage was described in 1864 by an outstanding domestic surgeon N. I. Pirogov: "With a torn hand or a foot, there is such a selection on the dressing point still .. He does not shout, does not cry, does not complain, does not accept any participation And nothing requires: the body is cold, the face is pale, like a corpse; The view is still and addressed in the distance; Pulse, like a thread, barely noticeable under the finger and with frequent jams. It is not answered for questions to the questions, or only to yourself a little heard with a whisper, breathing is also barely not enough. Rana and skin are almost insensitive. " The described features indicate the ongoing activation of the sympathoadrenal system (pale, cold skin, tachycardia) and about the oppression of the function of the central nervous system (the consciousness is darkened, although completely and not turned off, the inhibition of pain sensitivity). The leading pathogenetic links are painful irritation and developing hypovolemia.

Dehydration shock.It arises as a consequence of a significant dehydration of the body due to loss of fluid and electrolytes. With pronounced exudative pleuritic, Ileus, peritonite, the liquid from the vascular channel goes into the corresponding cavities. With an indomitable vomiting and a strong diarrhea, the fluid is lost outward. The consequence is the development of hypovolemia, which plays the role of a leading pathogenetic level. An additional acting factor is often an infectious process.

Burn shock.It occurs with extensive and deep burns covering more than 15% of the body surface, and in children and the elderly - even with smaller areas. At the same time, in the first 12-36 hours, the permeability of capillaries is increasing dramatically, especially in the burn zone, which leads tosignificant exit of fluid from vessels in tissue. A large amount of edema fluid, mainly in the place of damage, evaporates. With a burn, 30% of the body surface in an adult patient is lost with evaporation to 5 - 6 l per day, and the volume of circulating blood drops by 20-30%. The leading pathogenetic factors become hypovolemia, pain irritation, a pronounced increase in vessel permeability.

Cardiogenic shock.It occurs most often as one of the heavy complications of acute myocardial infarction. According to B03, it develops in 4 - 5% of patients under 64 years. Big role In the development of cardiogenic shock, the magnitude of the affected portion of myocardium plays. It is believed that it always develops with a damage to 40% and more mass of myocardium. It may occur under smaller volumes of myocardial damage in cases of attachment of additional complications, such as arrhythmias. It is possible to develop this type of shock and in the absence of a heart attack in cases of mechanical obstacles to filling or emptying ventricles, with a tamponade of the heart, intracardiac tumors. The cardiogenic shock is manifested by pain, up to an anginal state, arterial hypotension, although there are cases of normal blood pressure, activation of the sympathoadrenal system and peripheral signs of the perfusion disorders.

The leading pathogenetic links in the development of cardiogenic shock are: 1) painful irritation; 2) Violation of the contractile function of the heart and 3) violation of the rhythm of the heart. The severity and combination of these links in each case of cardiogenic shock are different, which gives grounds for the allocation of different forms of this complication. The result of a violation of the contractile function is to reduce cardiac output and as a result - reduction of the cardiac index. Hypovolemia develops. Accession of arrhythmia aggravates this process.

Septic (synonym: endotoxin) shock.It occurs as complication of sepsis. Hence the name "septic". Since the main damaging factor is endotoxins of microorganisms, this shock is also called endotoxin. The introduction of appropriate doses of endotoxins can be obtained by many changes arising during septic shock in humans. The most common cause of septic shock is gram-negative microorganisms - intestinal wand, klebseyella, streptococci, pneumococci.

A feature of septic shock is its development against the background of an existing infectious process and a primary septic focus, from which microorganisms and their toxins (cholangitis or pyelonephritis with the obstruction of withdrawing paths, peritonitis, etc.) are coming into the body. Shock is characterized by fever, chills with abundant sweating, tachycardia, tachipne, pale skin, rapidly progressive insufficiency of blood circulation, impaired lung function.

Leading pathogenetic links of shock: 1) an increase in the need of the body in the delivery of oxygen tissues. This is caused by fever (strengthening metabolic processes), increased operation of respiratory organs (Tahipne), chills. (Strengthening the operation of the skeletal muscles), an increase in the work of the heart - cardiac output increases by 2-3 times. The latter leads to a decrease in the total peripheral resistance of the vessels; 2) Reducing blood oxygenation in the lungs and insufficient extraction of oxygen from blood tissues. Oxygenation is reduced due to circulatory disorders in a small circle caused by microtromboembolia, aggregation of platelets on vessel spikes, as well as a violation of ventilation and perfusion relations in the lungs due to the development of atelectasis, pneumonia, edema. Insufficient extraction of oxygen from the blood is explained by several reasons: a) a sharp increase in shunt blood flow in tissues; b) in the early stages of respiratory alkalosis due to tachipne and caused by this shift of the dissociation curve of oxygemoglobin to the left; 3) Activation by endotoxins of proteolytic systems in biological fluids (kallicrein-kinine, complement, fibrinolytic) with the formation of products with a pronounced biological effect.

Anaphylactic shock.

Anaphylactic shock It flows as a whole standard: short erectile stage, after a few seconds - torpid. W. guinea Ginger - mostly spasm of the bronchi (asthmatic type of shock), in dogs - spasm of sphincters of hepatic veins, stagnation of blood in the liver and intestines - collapse, at the rabbit - mainly the spasm of pulmonary arteries and blood stagnation in the right half of the heart, in humans - all components: drop blood pressure Due to the redistribution of blood and violation of the venous return, the attack of suffocation, involuntary urination and defecation, skin manifestations: urticaria (uurticaria), swelling (ODEMA), itching (PRRITUS).

It differs from the remaining types of shock by the fact that the test mechanism in its pathogenesis is the antigen antibody reaction, as a result of which blood proteases are activated, they are released from the fat cells of histamine, serotonin and other vasoactive substances that cause primary dilatation of resistive vessels, lowering peripheral resistance and arterial hypotension. TO anaphylactic Gemotransfusion shock, where the main mechanism is the interaction of antigens of alien erythrocytes (incompatible on AB0 antibodies with serum antibodies) - as a result, agglutination of erythrocytes, their hemolysis + release of vasoactive substances → Dration of vessels + microcirculatory blocks by agglutinated red blood cells + damage to the epithelium of parenchymal organs hemolysis .

Principles of pathogenetic shock therapy (in negovsky). The fight against shock must be a complex, simultaneous and directed to the restoration of three systems: 1) nervous - to remove pain - blockades, anesthesia, craniocerebral hypothermia, 2) blood circulation recovery - drug infusion only in vessels or heart and no oral administrations (braking the absorption function and motorcycle gasts). Improve nutrition of nerve cells, prevent decortication. 3) Breathing - the fight against metabolic acidosis, abundant oxygenation + hyperbaric oxygenation, be sure to take into account the status of the victim.

"

Traumatic shock - the response of the body into a heavy mechanical injury, accompanied by a violation of all functions in the body.

Epidemiology.

Frequency of traumatic shock in the wounded in modern conditions Conducting hostilities increases, reaching 25%. The shock for multiple and combined damage is met in 11-86% of victims, which averages 25-30% of all accidents. Etiology.The most frequent causes of the development of traumatic shock: - damage to the pelvis, chest, lower extremities; - damage to the internal organs; - Open damage with an extensive scramble of soft tissues when the limbs are separated. Shock may occur with a varied combination of damage and even with multiple heavy bruises.

Pathogenesis.

As a result of severe injury or injury, one or several (with multiple or combined injuries) of foci of damage to fabrics or organs is formed. At the same time, vessels of various caliber are damaged - bleeding occurs , an irritation of an extensive receptor field occurs - a massive afferent effect on the central nervous system occurs, a more or less extensive volume of tissues is damaged, the products of their decay are absorbed into the blood - endotoxicosis occurs.

In case of damage to the vital organs, there is a violation of the corresponding vital functions: damage to the heart is accompanied by a decrease in the contractile function of myocardium; lung damage - decrease in pulmonary ventilation; Damage to the pharynx, larynx, trachea - asphyxia.

As a result of these pathogenetic factors on an extensive afferent receptor apparatus and directly on organs and tissues, a non-specific adaptation program for the protection of the body is launched. The consequence of this is the release of adaptation hormones into the blood: ACTH, cortisol, adrenaline, norepinephrine.

There is a generalized spasm of capacitive vessels (veins), providing the release of blood reserves from the depot - up to 20% of the BCC; Generalized spasm Arteriole leads to centralization of blood circulation and contributes to the spontaneous stop of bleeding; Tachycardia ensures that the proper blood circulation is maintained. If the severity of injury and blood loss exceed the protective capabilities of the body, and medical care is delayed - hypotension and tissue hypoperfusion develop , being clinical and pathogenetic characteristics of traumatic shock III degree.

Thus, the mechanism for the development of traumatic shock monoethiological (injury), but polypatogenetic (bleeding, endotoxicosis, damage to vital organs, afferent impact on the central nervous system), in contrast hemorrhagic Shock (for example, with key-cut wounds with damage to large vessels), where the pathogenetic factor is one - acute blood loss.

Diagnosis and classification of traumatic shock.

During the traumatic shock, two phases are distinguished: erectile and torpid.

• Erectile phase Relatively short. Its duration ranges from a few minutes to several hours. Patient in consciousness, troubled. Motive and speech excitement. Violated the criticism of the assessment of your own state. Pale. Pupils of ordinary sizes, the reaction to the light is alive. Pulse of good quality, rapidly. Blood pressure within the normal range. Increased pain sensitivity and skeletal muscle tone.
• Thorpid phase The shock is characterized by the oppression of vital functions of the body and, depending on the severity of the flow divided by three degrees:

— shock I degree. Consciousness is preserved, there are easy inhibition and slowness of the reaction. Pain reaction is weakened. Skin pale, acrocyanosis. Pulse of good quality, 90-100 per minute, systolic blood pressure 100-90 mm Hg. Light tachipne. Skeletal muscles tone reduced. Diuresis is not broken.

— shock II degree. By clinical picture It is similar to a shock of I degree, but is characterized by a more pronounced oppression of consciousness, a decrease in pain sensitivity and muscle tone and significant impairment of hemodynamics. Pulse of weak filling and voltage - 110-120 per minute, maximum blood pressure 90-70 mm Hg.

— shock III degree. Consciousness is darkened, the patient sharply slow down, the reaction to external stimuli is noticeably weakened. Skin covers pale gray, with a blue tint. Pulse of weak filling and voltage, 130 per minute and more. Systolic blood pressure 70 mm Hg. And below. Surface breathing, frequent. Muscular hypotension, hypotlexia, decreased diurea, up to Anuria. Great diagnostic value In determining the degree of shock, the Algover index is played: the ratio of heart rate to the level of systolic blood pressure. It is possible to approximately determine the degree of shock and the size of the bloodsture (Table 3).

Shoka Index

The late elimination of the reasons for supporting and deepening traumatic shock prevents the restoration of the vital functions of the body, and the III shock of the degree can go to the terminal state, which is the extreme degree of oppression of vital functions passing into clinical death.

Principles of medical care:

- the urgent nature of the provision of medical care for traumatic shock, due to the threat of irreversible consequences of critical disorders of vital functions and, above all, circulatory disorders, deep hypoxia.

- the feasibility of a differentiated approach in the treatment of wounded in a state of traumatic shock. Treated should not shock as
Such, not a "typical process" or "specific pathophysiological reaction". The anti-coaxing assistance turns out to be concrete wounded with hazardous violations of vital activity, which is based on severe injury ("Morphological substrate" of shock) and, as a rule, sharp blood loss. Pronounced circulatory disorders, respiration and other vital functions are caused by severe morphological damage to vital organs and organism systems. This position in severe injuries acquires the meaning of the axioms and aims the doctor to urgently search for a specific cause of traumatic shock. Surgery with shock is effective only with the rapid and accurate diagnosis of localization, nature and severity of damage.

- leading importance and emergency nature of surgical treatment with traumatic shock. The anti-shifting assistance is simultaneously an anesthesiologist-resuscitation and surgeon. From effective action The first depends on the rapid restoration and maintenance of respiratory tract, gas exchange as a whole, the beginning of infusion therapy, anesthesia, medical support for cardiac activity and other functions. However, pathogenetic meaning has urgent surgical treatment, eliminating the cause of the traumatic shock - stopping bleeding, eliminating the tense or open pneumothorax, elimination of the tamponade of the heart, etc.

Thus, the current tactics of active surgical treatment of the seriously edged occupies a central place in the program of anti-shock events and does not leave the place to the outdated thesis - "First bring out of the shock, then operate." A similar approach proceeded from incorrect ideas about traumatic shock as a purely functional process with predominant localization in the central nervous system.

Anti-shock events at the stages of medical evacuation.

The first and prefiguration assistance includes:

• Stop outdoor bleeding by temporary methods, to the wounds to impose aseptic bandages.
• Analgesic injection with syringe - Tubes.
• Immobilization of fractures and extensive damage by transport tires.
• Elimination of mechanical asphyxia (exemption of the upper respiratory tract, overlaying an occlusal bandage with pneumothorax).
• Early start of infusion of bloodstream solutions using field disposable plastic infusion systems.
• The priority careful transportation was injured for the next stage.

First medical care.

The wounded in the traumatic shock should first be directed into the dressing room.

Anti-slip assistance should be limited to the necessary minimum of urgent measures, so as not to delay the evacuation into a medical institution where surgical and resuscitation assistance can be provided. It should be understood that the purpose of these events is not to eliminate from shock (which is impossible under conditions under conditions), but stabilization of the state of the wounded for further priority evacuation.

The dressing reasons are detected by the causes of the difficult state of the wounded and perform measures to eliminate them. With acute respiratory disorders — the asphyxia is eliminated, the external breathing is restored, the pleural cavity is sealed with an open pneumothorax, the pleural cavity with a strained pneumothorax is drained, inhalation of oxygen is carried out. With outer bleeding, its temporary stop is performed, and in the presence of a hemostatic harness - a harness is controlled.

An intravenous infusion is carried out 800-1200 ml of crystalloid solution (Mafusol, lactasol, 0.9% solution of sodium chloride, etc.), and with massive blood loss (2 l and more), additional infusion of the colloidal solution (polyglyukin, etc.) in the amount of 400 -800 ml. Infusion continues in parallel with the implementation of medical measures and even during the subsequent evacuation.

The obligatory anti-deposit event of the first medical care is anesthesia. All wounded with traumatic shock are introduced narcotic analgesics. However, the best method of anesthesia is novocaine blocks. Transport immobilization is monitored. When internal bleeding, the main task of the first medical care is the organization of immediate evacuation of the wounded to the stage of providing qualified or specialized medical care, where it will be implemented by an emergency operation to eliminate the source of bleeding.

Qualified and specialized assistance.

The wounded with the signs of the shock should first be sent to the operating room for emergency operations (asphyxia, tamponade of the heart, stressful or open pneumothorax, continuing internal bleeding, etc.) either in the ward of intensive therapy for the wounded - in the absence of indications for an emergency operation ( To eliminate disorders of vital functions, preparation for the performance of urgent surgical interventions or evacuation).

In the wounded, in need of urgent operations, anti-shutter therapy should begin in the receiving and sorting department and continue under the leadership of the anesthesiologist-resuscitator simultaneously with the implementation surgical intervention. In the future, after surgery, the anti-mask therapy is completed in the ward of intensive therapy. The average dedication period of the wounded from the state of the shock at war is 8-12 hours. At the stage of specialized assistance after removing from the shock, the wounded with the terms of treatment not exceeding 60 days is carried out a full course of treatment. The rest of the wounded evacuate into the rear hospital.

Popkov V. M., Chesnokova N. P., Ice Ice, M. Yu.,

2.1. Traumatic shock, etiology, developmental stages, pathogenesis

Before you give the definition of shock, I would like to recall the well-known Deloyers expression: "Shock is easier to recognize than to describe, and it is easier to describe what to give it a definition."

Traumatic shock is an acute neurogenic insufficiency of peripheral circulation, which occurs under the influence of an emergency traumatic factor, combined with phase violations of the central nervous system, hormonal balance, corresponding to metabolic and functional disorders of various organs and systems.

The proposed determination of traumatic shock, of course, cannot claim to absolutely complete the characteristics of the entire complex of disorders characteristic of traumatic shock, and can be largely supplemented by the definition of the shock that G.I. Nazarenko (1994): Traumatic shock is a typical evolutionary formed, a phase developing pathological process of an acute period of traumatic disease.

Features of clinical manifestations of traumatic shock, the severity of its flow is determined largely by the nature of the injury inducing the development of shock. In this regard, it is necessary to note the diversity of the classifications of traumatic shock, reflecting in the main nature of injury, its severity and localization.

So, in a number of manual, traumatic shock includes the following varieties of shock:

1) surgical shock;

2) shock caused by burn;

3) shock caused by the imposition of a harness;

4) shock caused by fragmentation;

5) shock caused by a drum air wave;

6) endotoxin shock.

Proposed by VK. Kulagin (1978) The classification of traumatic shock is relevant to the present moment and includes the following varieties of traumatic shock:

a) the wound arising from heavy mechanical injuries, including the components of the pain and mental species shock. Depending on the localization of the injury is divided into the following forms: cerebral, pulmonial, visceral, during the injury of limbs, with long-term squeezing of soft tissues, with multiple injury;

b) hemorrhagic, arising from external and internal bleeding;

c) operational;

d) mixed.

In the dynamics of traumatic shock, most researchers starting with N.I. Pirogov, allocate two stages of development: erectile (excitation) and torpid (braking), characterizing essentially functional state of the central nervous system. In the case of an unfavorable flow of traumatic shock at the end of the trapid phase, a terminal state comes. In terminal state, depending on the nature and severity of functional disorders and the nature of clinical manifestations, the preagonia, agony and clinical death differ.

The erectile stage of shock occurs directly after the impact of the traumatic factor; Its duration is a few minutes, and therefore patients with traumatic shock are delivered to the hospital in the braid stage of shock. The duration of the shock of the shock is, as a rule, from several hours to two days.

The leading pathogenetic factors of traumatic shock are: intensive pathological affamentation with various receptor zones, in particular, with pain and tactile receptors of injury, psycho-emotional stressing, rapidly developing endogenous intoxication, reduction of circulating blood volume and, finally, violating the structure and functions of various organs and Tissues characteristic of the so-called polyorganic failure at shock.

Touching the pathogenesis of the erectile stages of shock, the general patterns of the formation of stress reactions should be noted, to which traumatic shocks detected by the city of Siele and received confirmation in numerous studies of domestic and foreign authors.

As it is known, the flow of afferent impulsation from various interim, extero and proproportors, which is generated during the effects of injury to the body, is applied to the rising spinocortical paths not only to the relevant cerebral centers, but, above all, to the reticular formation of the brain barrel, the limbic system. The activation of the reticular formation of the brain barrel is accompanied by the strengthening of ascending and descending activating influences on the bark of the brain, the centers of the oblong brain, hypothalamic structures, spinal engine centers, which causes the development of the erectile shock phase. The characteristic signs of the erectile phase developing directly follow the action of the traumatic factor are: common speech and motor excitation, pallor of skin, sometimes involuntary urination and defecation.

Strengthening activating influences on the bulbar vessels, leads to a short-term increase in neurogenic vascular tone and, accordingly, blood pressure. Non-specific activation of the bulbar respiratory center in the erectile stage of shock is manifested by the development of Tahipne.

At the same time, the activation of the hypothalamus, structurally and functionally closely interconnected with bulbar reticular formation. The activation of the rear hypothalamic structures, including the highest vegetative centers of the sympathetic system, entails a cascade of reactions characterized by a change in the neurohumoral regulation of the activities of a number of internal organs and systems.

When the sympathetic system is activated in the erectile stage of shock, positive inotropic and chronotropic effects On the heart, tachycardia arise, hypertension. At the same time, the spasm of the renal chicken vessels is developing, which leads to the activation of the renin-angiotensin system, the products of angiotensin-II, which has a pronounced vasoconstrictor effect, is enhanced.

The activation of the front and middle departments of the hypothalamus in the erectile stage of traumatic shock is accompanied by an increase in the production of antidiuretic hormone with a suprasoptic nucleus of the front hypothalamus and its secretion into the systemic bloodstream, as well as the formation of so-called liberins, in particular, corticoliberine and thyrolyiberin. The latter hyumoral means have an activating effect on adenogipophysis and, accordingly, lead to an increase in the products of adrenocorticotropic and thyrotropic hormones. However, it should be noted that the intensification of the products of the thyrotropic hormone in stressful influences is not indisputable fact.

One of the important links of adaptation reactions that are formed already in the erectile stages of shock is the activation of the release of the beam zone of the glucocorticoid adrenal cortex under the influence of the adrenocorticotropic hormone. At the same time, the products of mineralocorticoids of the glomerular zone of the adrenal cortex are styled against the background of the activation of the renin-angiotensin system.

Characteristic changes undergoes the incremental function of the pancreas in the erectile and subsequent trapid stages of shock. Against the background of the activation of the sympatholic system in the erectile stage of the shock, the glucagon hyperproduction occurs, selective inhibition of insulin secretion. However, the hyperglycemia occurs simultaneously against the background of these hormone shifts is a factor stimulating insulin products.

Instantly developing hormonal imbalance in the erectile stage of shock is accompanied by the emergence of a complex of metabolic and functional disorders that are even more increasing in the depletion stage of the shock.

Catecholamine hyperproduction leads to activation of glycolysis and glycogenolysis enzymes, in particular, phosphorylase and glucose-6-phosphatase liver, which is accompanied by the development of hyperglycemia, and in some cases and glucosuria, that is, symptomatics of so-called post-traumatic diabetes mellitus.

Excessive products of glucocorticoid leads to activation of catabolic reactions, the protein decay processes in lymphoid, muscle tissues are enhanced, negative nitrate balance occurs. At the same time, the processes of glukegenesis in the liver are stimulated, providing a sufficiently long-term hyperglycemic response in response to the action of the traumatic agent.

The enhancement of adrenergic effects on various organs and tissues in the erectyl stage of shock leads to the spasm of peripheral vessels, limiting blood flow, the development of ischemia and hypoxia, expressed largely in the skin, skeletal muscles, abdominal organs. Vasoconstrictor effects of catecholamines are potentiated in the dynamics of the development of shock due to hyperproduction of vasopressin and angiotensin-II. Oxygen deficiency in the tissues is enhanced by both activation under the influence of catecholamines and glucocorticoids of glycolysis, lipolyase processes, proteolysis, which leads to an excessive accumulation of acidic products: dairy, peer-grade, fatty acids, ketokislot, amino acids, the further metabolism of which in the cycle of tricarboxylic acids is impossible in connection with circulatory hypoxia.

Currently, it is a generally accepted fact of centralizing blood circulation arising against the background of pronounced peripheral vasoconstrictions. The centralization mechanisms of blood flow are formed in the erectile stages of shock, although they continue to provide it at the initial stages of the shock of the shock. The centralization of blood flow is maintained by dilatation of blood vessels, brain, adrenal glands and pituitary glands mainly by increasing the activity of the sympatholic system.

Thus, despite the short-term development, the erectile stage of shock plays an extremely important role in the induction of the reactions of deadaption, the peopide stage of traumatic shock, as well as to ensure endogenous mechanisms of antistress protection of the body. It is in the erectile stages of shock that mechanisms are deployed, providing the formation of pathological deposit of blood, insufficiency of peripheral blood circulation, as well as transformations of the erectile stages of shock in a torpidal one.

So, what are the clinical manifestations of the shock stage and the mechanisms of their development?

A classic description of the trapid stage of traumatic shock was given by N.I. Pirogov in 1865, "with a torn hand or a foot lies with such a stool on the dressing point stationary; He does not shout, not crying, does not complain, does not take into account anything and does not require anything; The body is cold, the face is pale, like the corpse, the view is still and addressed in the distance; Pulse- like a thread, barely noticeable under the fingers with frequent jams. Okocheny or not answers questions, or only to yourself, a little heard shopot; Breathing is also barely noten. The wound and the skin are almost not sensitive at all, but if the sick one with one slight reduction of personal muscles detects signs of feeling ... "

From a modern point of view, in the development of the trapid stage of traumatic shock in accordance with the state of the parameters of hemodynamics, two phases are made: compensation and decompensation. Phase compensation is characterized the following manifestations: Cold wet skin, progressive tachycardia, pallion of mucous membranes, relatively high blood pressure, lack of pronounced hypoxic changes in myocardium according to ECG data, lack of signs of brain hypoxia. Pupils can be somewhat expanded by increasing the tone of radial muscles due to the activation of the sympathetic system. The duration of the content of capillaries under the nail lies, the so-called symptom of stains, more than 3-5 seconds. To assess the degree of severity of the turnup stage of the shock, the use of a rectal skin gradient is recommended, which is an integrative indicator of the microhemocirculation state. This test is easily reproducible in any conditions, is characterized by a difference between the temperature in the lumen of the rectum at a depth of 8-10 cm and the temperature of the skin on the rear of the foot at the base of the 1st finger. Normally, the rectal skin gradient is 3-5 ° C. Increasing this gradient over 6-7 ° C testifies to the development of shock. G.I. Nazarenko (1994) notes that the observation of the dynamics of this gradient allows us to evaluate the effectiveness of anti-aggregate therapy. If, despite the set of events, this gradient continues to increase, the forecast of the shock state becomes less favorable, an increase in the skin-rectal gradient over 16 ° C indicates the possibility of developing death in 89% of cases.

In the compensation phase of the shock, this gradient increases insignificantly. Central venous pressure in this phase is normal or somewhat reduced.

In this way, characteristic features Phases of compensation of the depletion stage of shock are: the pronounced activation of the sympathetic system with characteristic functional and metabolic shifts characteristic, in particular, the development of tachycardia and the hypendynamic nature of blood circulation. During this period, the centralization of blood flow is still quite expressed, there are no hypoxic changes in the myocardium and in the structures of the brain, the pressing reaction to intravenous administration of norepinephrine is preserved, the spasm of peripheral vessels of the skin, skeletal muscles, abdominal organs is expressed.

However, already in the compensation phase of the traumatic stage of traumatic shock, the mechanisms of deadaption, decompensation are intensively deployed. The phase of compensation for the traumatic shock of the traumatic shock is characterized by the depletion of the adaptive capabilities of the body, which is manifested by the hypodynamic nature of blood circulation, arise a progressive decrease in the minute volume of blood, hypotension, microcirculation crisis characterized by the development of thrombosis phenomena, hemorrhagium, solicing the erythrocytes. At the same time, the refractoriness of the microsuds to the nervous and humoral vasoconstrictor influences occurs.

Microcirculation disorders in the phase of decompensation of traumatic shock are characterized by the progressive pathological deposit of blood.

Concerning the mechanisms of the development of pathological deposit of blood should be noted that they are formed already in the erectile phase of shock, develop in the compensation phase of the shock of the shock and reach the maximum in the phase of decompensation of the shock stage.

Pathological deposition of blood exacerbates the imbalance between the capacity of the vascular bed and the volume of circulating blood, that is, it is an essential pathogenetic factor in the development of a shock state characterized by non-regional blood flow and microcirculation.

So, in the erectile stages of shock due to the activation of the sympathoadrenal system, the renin-angiotensin system, the enhancement of exemption in synaptic structures or blood flow, adrenaline, angiotensin-II, glucocorticoids, occur spasm of pre- and post-checkillers of peripheral organs and tissues, reducing the blood flow rate Through the capillaries, aggregation of red blood cells mainly in Veneulah. At the same time, naturally, circulatory hypoxia occurs, accompanied, in turn, by a complex of secondary nonspecific metabolic and functional shifts. In particular, the processes of free radical oxidation are activated in the hypoxia zone, unsafected methods of metabolism begin to accumulate, formed initially compensated, and then decompensated metabolic acidosis. In the conditions of acidosis, a complex of compensation and damage reactions arises.

Secondly, the phenomena of the degranulation of fat cells are noted, highly active compounds, in particular, histamine, serotonin, leukotrienes, heparin, factor of platelet aggregation factor, the factors of chemotaxis neutrophils are observed in excess, etc., many of which have vasoactive action, Cause an expansion of the vessels of the microcirculatory bed, increasing the permeability of the vascular wall, the development of plasmopotier and subsequent thickening of blood.

It should be noted that under the influence of the excess of hydrogen ions in peripheral organs and tissues, destabilization of membranes lysosomes occurs, which leads to the exit into the extracellular medium of a large number of lysosomal enzymes. The latter cause the destruction of protein, lipid, carbohydrate components of cell membranes and intercellular substance of the connective tissue. The activation of phospholipase with lysosomes is accompanied by an increase in the products of polyunsaturated fatty acids, the substrate activation of cycoxicenase and lipoxygenase enzymes, and therefore the intensive synthesis of prostaglandins and leukotrienes begins with a pronounced vasodilator effect that increase the permeability of the vessels that induce the development of plasmopotier, blood thickening. Damage to the endothelium of the vessels in the zone of circulatory hypoxia, the exposure of collagen of the vascular wall is accompanied by the enhancement of the processes of adhesion and platelet aggregation, as well as activation of internal and external mechanisms The formation of pritrontinase activity, that is, the prerequisites for the development of thrombohemorrhagic syndrome are created.

Under the influence of excess of hydrogen ions, the opening of arteriolienular shunts and the phenomenon of the new formation of capillaries, not functioning under the conditions of the norm, increase the capacity of the vascular bed. It should be noted that the discharge of blood through arteriovenous shunts aggravates the state of hypoxia, since they do not provide transmembrane metabolism with tissues.

Thus, combined effects of excess of hydrogen ions, as well as a complex of biologically active compounds in the peripheral vasoconstriction zone, induced by the activation of adrenergic effects, determine a sharp increase in the capacity of the microcirculatory stream, the loss of elasticity of microsudes, increasing their permeability, which will ultimately increase the development of pathological deposit of blood and shock state. Pathological blood deposit initially develops in the microsudes of the injury, skin, subcutaneous tissue, muscle tissue, intestines, and with long hypoxia, and in the liver, kidneys, pancreas.

In connection with the development of pathological deposit of blood, the plasmopoterer arises thickening of blood, the volume of circulating blood decreases sharply, the venous return is reduced. The decline in venous return leads to the further stimulation of the sympathetic system, tachycardia is even more aggravated. At the same time, the time of diastole and the diastolic filling of the cavities of the heart decreases dramatically, the heart rate falls, blood pressure drops, the shock syndrome is aggravated.

Thus, the basis of the shock state lies the imbalance between the volume of circulating blood and the capacity of the vascular channel, when the capacity of the vascular channel has a tendency to progressive increase in the shock dynamics, and the volume of circulating blood decreases sharply. The drop in the volume of circulating blood in the dynamics of traumatic shock, as mentioned above, is due to a complex of pathogenetic factors: possible blood loss, mandatory plasmopoter in connection with an increase in the permeability of the vascular wall of the microcirculatory bed of various peripheral organs and tissues, pathological deposition of blood, a decrease in systolic ejection as a consequence of a decrease in venous return and the activation of the sympathetic system.

One of the key problems of diagnosis and treatment of shock in severe injuries is the correctness of the gravity of the traumatic shock in the traumatic phase.

Currently, there are various criteria for hemodynamic disorders, including using methods for evaluating cardiac output, oxygen flux and degree of hypoxia, osmolarity and colloid-osmotic plasma pressure, plasma volume, metabolic disorders, coagulation status, water and electrolyte balance and function kidneys, respiratory function of the lungs, etc.

However, in emergency clinical practice, generally accepted integrative criteria for the gravity of hemodynamic disorders are often used at shock - the size of the blood pressure and the rate of the pulse.

The most common is the classification of severity of the flow of shock on the size of systolic pressure: a pressure of 90 mm Hg. Art., indicates a shock of the 1st degree, 85-75 mm Hg. Art. - About shock 2nd degree, 70 mm Hg. And below - about the shock of the 3rd degree.

The almedic index is also used to assess the gravity of hemodynamic disorders, which is the ratio of the pulse rate to the magnitude of systolic blood pressure. Under the conditions of the norm, the specified indicator is 0.5-0.6, with a shock of 1st degree - 0.7-0.8, 2nd degree - 0.9-1.2, 3 degrees - 1.3 and higher.

To develop the principles of pathogenetic therapy of shock, it is necessary to clearly imagine the mechanisms for the development of the traumatic stage of traumatic shock, pathogenetic factors resulting in the transformation of the erectile stages of shock in the torpid.

For a long time, the point of view was existed according to which the transformation of the erectyl stage of shock in the turpentine occurs due to progressive hemodynamic disorders, pronounced circulatory hypoxia initially in the peripheral organs and tissues, and as the pathological deposit of blood and the falling of blood pressure, which takes place in the structures of the brain and heart. It should be noted that the fact of progressive circulatory hypoxia in the dynamics of traumatic shock is indisputable, and in hypoxia, it is known, the formation of free radicals increases, disintegration of biological membranes, the deficit of macroehers, is suppressed, all energy-dependent responses in cells, including transmembrane transfer of ions. , Cell depolarization phenomena arise, their excitability changes and, accordingly, functional activity.

However, despite the above pattern of metabolic shifts and hemodynamic disorders, which cause the transformation of the erectile stages of shock into a torpid, not all researchers note the instantaneous depletion of energy substrates in the brain tissues in the erectile stages of shock, while the level of ATP remains normal even in the braid stage of shock.

In the transformation mechanisms of the erectile stage of shock, a torpidal role should be assigned to pronounced disorders of the neurogormonal and humoral regulation of the function of organs and systems. The sharp activation of the hypothalamic-pituitary-adrenal system in the erectile stages of shock, the strengthening of the production of hormones ACTH and glucocorticoids is accompanied by the intensification of glucocorticoid metabolism in tissues and as fast depletion of the beam zone of adrenal cortex and the products of glucocorticoids, respectively. Under the conditions of the relative deficit of glucocorticoids, many non-specific adaptation reactions are suppressed, characteristic of stress syndrome, including basal vascular tone, progress the shock state, circulatory hypoxia and its associated polyorgan failure.

At the same time, excessive activation of the sympathetic system in the erectile stage of shock induces the inclusion of endogenous anti-stress protection mechanisms - the synthesis in the structures of the brain is enhanced, in various internal organs and tissues of brake mediators, in particular, gamma-amine oil and gamma hydroxyma salts, prostaglandins of the group E, Opioid neuropeptides, which, in turn, limit the stress reaction, however, released in inadequate concentrations, can exacerbate hemodynamic disorders characteristic of shock states, and, accordingly, the severity of clinical manifestations of shock.

We bring to your attention the magazines publishing in the publishing house "Academy of Natural Science"

Traumatic shock (etiology, pathogenesis)

Traumatic shock is an acutely developing due to injury, a polypatogenetic pathological process, characterized by significant violations of the functions of life support systems, primarily blood circulation, against the background of the extreme voltage of regulatory (adaptation) mechanisms of the body. Traumatic shock is one of the manifestations of the acute period of traumatic disease. The polyethology of the traumatic shock is determined by the fact that its formation occurs as a result of the interaction of circulatory disorders caused by blood loss; disorders of the pulmonary and tissue gas exchange; the organism poisoning with products of destroyed tissues and impaired metabolism, as well as toxins of microbial origin; powerful stream of neuroral pulses from the damage zone in the brain and the endocrine system; violations of the function of damaged vital organs.

The main link pathogenesis of traumatic shock are primary disorders of microcirculation. Acute insufficiency of blood circulation, lack of perfusion of tissues with blood leads to inconsistencies between reduced microcirculation capabilities and energy needs of the body. At traumatic shock, in contrast to other manifestations of the acute period of traumatic disease, hypovolemia due to bloodstures is the lead, although not the only reason for hemodynamic violations.

An important factor determining the state of blood circulation is the work of the heart. For most victims with severe injuries, the development of a hypendynamic type of blood circulation is characteristic. With a favorable course, its permanent volume after injury can remain elevated throughout the acute period of traumatic disease. This is due to the fact that coronary arterys are not involved in the common vascular spasm, it remains satisfactory venous return, cardiac activity is stimulated through vascular chemoreceptors of unsophisticated exchange products. However, with a preserving hypotension, after 8 hours after injury, a single and minute heart performance in patients with traumatic shock can decrease by about twice as compared to the norm. The increase in the heart rate and the total peripheral resistance of the vessels is not able to maintain a minute volume of blood circulation on normal values \u200b\u200b(Pashkovsky E.V. et al., 2001).

Insufficient cardiac release at traumatic shock is due to the depletion of urgent copins mechanisms due to myocardium hypoxia, the development of metabolic disorders in it, a decrease in the content of catecholamines in myocardium, a decrease in its reaction to sympathetic stimulation and catecholamines circulating in blood. Thus, the progressive decrease in one-time and minute performance of the heart will be a reflection of developing heart failure, even in the absence of direct damage (injury) of the heart (V.V. Timofeev, 1983).

Another main factor determining the state of blood circulation is the tone of the vessels. A regular reaction to injury and blood loss is the strengthening of the functions of a limbico-reticular complex and a hypothalamic-adrenal system. As a result, the traumatic shock includes urgent compensatory mechanisms aimed at maintaining blood circulation of vital organs. One of the compensation mechanisms is to develop a common vascular spasm (first of all arterioles, metharcyteries and prokapillary sphincters) aimed at emergency decrease in the capacity of the vascular bed and bring it into line with the BCC. The total vascular reaction does not apply only on the artery of the heart and brain, which are practically deprived of? -Adrenoreceptors implementing the vasoconstrictor effect of adrenaline and norepinephrine.

The mechanism of urgent compensation, also aimed at eliminating the inconsistency between the BCC and the capacity of the vascular bed, is autogriego. In this case, the reinforced movement of the fluid from the interstitial space in the vascular is. The fluid yield in interstics occurs in functioning capillaries, and its entry goes to non-functioning. Together with interstitial liquid in capillaries penetrate the products of anaerobic metabolism, which reduce sensitivity? -Adrenororeceptors to catecholaminams. As a result, non-functioning capillaries expand, and functioning, on the contrary, narrow. With a shock due to an increase in the concentration of adrenaline and norepinephrine, the ratio between the functioning and non-functioning capillaries is dramatically changed in favor of the latter. Thus, conditions are created to increase the reverse current of the fluid into the vascular channel. Autohemodiliation is also amplified by the dominance of oncotic pressure not only in venular (as under normal conditions), but also in the arterilar ends of functioning capillaries due to a sharp decrease in hydrostatic pressure. The mechanism of autoghemodilia is quite slow. Even with bloodwall exceeding 30-40% OCC, the rate of flow of fluid from an interstice into the vascular channel does not exceed 150 ml / h.

In the reaction of urgent compensation of blood loss, a renal mechanism of water and electrolyte delay has a certain meaning. It is associated with a decrease in the filtering of the primary urine (decrease in filtration pressure in combination with spasm of renal vessels) and an increase in the reabsorption of water and salts in the tubing apparatus of the kidneys under the action of antidiuretic hormone and aldosterone.

In the exhaustion of the above-described compensation mechanisms, microcirculation disorders are progress. Intensive separation of histamine, bradykinin, lactic acid with damaged and stylish tissues with vasodilatory action; admission from the intestine of microbial toxins; The decline due to hypoxia and acidosis of the sensitivity of smooth muscle elements of the vessels to nervous influences and catecholaminams leads to the fact that the phase of vasoconstriction is replaced by the phase of vasodilation. There is a pathological deposit of blood in those who have lost the tone of metharrioles and extended capillaries. Hydrostatic pressure in them increases and becomes more oncotic. Due to the influence of endotoxins and hypoxia of the vascular wall itself, its permeability increases, the liquid part of blood leaves in interstics, the phenomenon of "internal bleeding" occurs. The instability of hemodynamics, violation of the tone of the vessels due to damage to the regulatory function of the brain in such a form of an acute period of traumatic disease, as a traumatic coma (severe crank-brain injury, the injury of a severe brain) usually develop later - by the end of the first day.

An important link of pathogenesis of traumatic shock, even with non-cleaning injury, is an acute respiratory failure. In character, it is usually parenchymal and ventilation. The most typical manifestation is the progressive arterial hypoxemia. Reasons for the development of the latter are the weakness of respiratory muscles under conditions of circulatory hypoxia; pain "brake" breathing; Embolization of the microShosudes of the lungs due to intravascular coagulation, fat globul, the yatrogenation of transfusions and infusions; interstitial pulmonary edema due to increasing the permeability of the membranes of microscopes of endotoxins, hypoxia of the vascular wall, hypoproteinemia; Microelectsization due to reducing the formation and reinforced destruction of the surfactant. The predisposition to the atelectasis, the tracheoobronchitis and pneumonia is exacerbated by the aspiration of blood, gastric content, increasing the release of mucus with bronchial glands, the difficulty of flipping against the background of insufficient blood supply to the tracheobronchial tree. The combination of pulmonary, hemic (due to anemia) and circulatory hypoxia is a key point of traumatic shock. It is hypoxia and tissue hypoperfusion that determine the metabolic disorders, immune status, hemostasis, lead to increasing endotoxicosis.

In victims with severe breast injury (multiple fractures of ribs, the formation of the rib valve, a tense pneumothorax, injury injury) in combination with a non-heavy trauma of other anatomical regions, the acute period of traumatic disease is primarily a sharp respiratory failure. For such affected are characteristic normal numbers Systolic blood pressure (more than 100 mm Hg. In addition, when this contingent of patients has an increase in the fibrinolytic blood activity due to the activation of the plasminine system as a result of damage pulmonary fabric. The predominance of hypercoagulation with the consumption of antosverting factors in arterial blood over venous against the background of the oppression of fibrinolytic activity plays a significant role in the pathogenesis of respiratory distress syndrome.

The role of nociceptive impulsation in the etiopathogenesis of traumatic shock is also very significant. It is based on the basis of the flow of nociceptive impulses, a stress reaction of the body is largely formed in response to injury. In its genesis, an afferent impulse with interoceptors of the cardiovascular system is essential, especially with a decrease in the OCC caused by acute massive blood loss.

The deepening of metabolic disorders, microcirculation disorders during traumatic shock is associated with endotoxicosis, which begins to appear after 15-20 minutes. After injury or injury. Optional and obligate endotoxins are medium molecular polypeptides (simple and complex peptides, nucleotides, glycopeptides, humoral regulators, derivatives of glucuronic acids, fragments of collagen and fibrinogen). The middle molecules pool is an important, but not the only supplier of toxic substances. The final toxic properties have finite spree products of protein, especially ammonia. Endotoxicosis is also determined by free hemoglobin and myoglobin, peroxide compounds. The immunoreaction arising from shock is not only protective, but can also act as a source of toxic substances, such as pro-inflammatory cytokines (protein or polypeptide compounds produced by activated cells immune system) - Interleukin-1, tumor necrosis factor, etc.

The essence of immune disorders at traumatic shock is associated with extremely high risk. early Development immune failure. For traumatic shock, an unprecedented high antigenemia from the foci of alteration of fabrics is characteristic. The barrier function of local inflammation is lost, and its mediators (pro-inflammatory cytokines) come into systemic blood flow. Under these conditions, the adaptive reaction of the immune system should be the so-called "preimmune response", when the level of pro-inflammatory cytokines is subtly controlled by the production of anti-inflammatory cytokines. With the unfavorable course of the acute period of traumatic disease, the scale of damage and the volume of foci of development of the inflammatory response does not allow the body to use this adaptation reaction. As a result, immune failure is developing with a decrease in the number and development of the functional insufficiency of cells involved in immune reactions, on the background of an imbalance in the regulatory link of immune homeostasis.

The central metabolic reaction at traumatic shock is hyperglycemia. It is due to the increase in the ranks of catecholamines, somatotropic hormone, glucocorticoids and glucagon. Due to this, glycogenolysis and gluconeogenesis is stimulated, the synthesis of insulin and its activity is reduced mainly in muscle tissue. Glucose synthesis enhancement is an urgent compensatory reaction, indicates an increased energy request for tissues. Due to the reduction in the consumption of glucose in the muscles, the body "protects" glucose to ensure the energy of vital organs. Glucose is the only source of energy in anaerobic conditions, the main energy substrate to ensure the reparation of tissues. Other metabolic reactions typical of traumatic shock are hypoproteinemia due to enhanced catabolism, the output of low-dispersed fractions in interstics, disaming disorders and re-emission in the liver and acceleration of lipolysis due to the activation of lipases for converting neutral fat into free fatty acids - energy source.

The electrolyte disorders characteristic of traumatic shock appear to the loss of potassium ions by cells due to the inefficiency of the energy-intensive potassium-sodium pump, the delay in sodium ions of aldosterone, the loss of phosphorus cations due to the violation of the synthesis of ATP and the loss of chlorine anions due to the output of them to the gastrointestinal tract and Concentrations in the damage zone.

Tissue hypoxia leads to the accumulation of osmotically active substances (urea, glucose, sodium ions, lactate, pyruvate, ketone bodies, etc.), which is consistently causes hyperosmolability in cells, interstics, plasma and urine.

For victims in a state of traumatic shock, metabolic acidosis is characterized, which takes place in 90% of patients, and in 70% of them, this disruption of the acid-base state is noncompensated.