General disorders of vital activity in surgical diseases. KSMU Department of General Surgery Critical Vital Disorders in Surgical Patients. VII. Questions for self-control

1. Types of violations of the body's vital functions. Shock, terminal states, acute respiratory, renal, cardiovascular insufficiency in surgical patients.

Shock- an acute critical condition of the body with a progressive insufficiency of the life support system, due to acute circulatory failure, microcirculation and tissue hypoxia.

In shock, the functions of the cardiovascular system, respiration, kidneys change, the processes of microcirculation and metabolism are disturbed. Shock is a polyetiological disease. Depending on the cause of occurrence, the following types are distinguished.

1. Traumatic shock: a) as a result of mechanical trauma (wounds, bone fractures, tissue compression, etc.); b) burn shock (thermal and chemical burns); c) when exposed to low temperature - cold shock; d) as a result of electrical injury - electric shock.

2. Hemorrhagic or hypovolemic shock: a) bleeding, acute blood loss; b) acute violation of the water balance - dehydration of the body.

3. Septic (bacterial-toxic) shock (common purulent processes caused by gram-negative or gram-positive microflora).

4. Anaphylactic shock.

5. Cardiogenic shock (myocardial infarction, acute heart failure)

Varieties and manifestations of terminal states.

Predagonal states;

clinical death.

In addition, grade III-IV shock has a number of signs characteristic of terminal states.

Terminal states most often develop as a result of acute blood loss, traumatic and surgical shock, asphyxia, collapse, severe acute intoxication (sepsis, peritonitis), coronary circulation disorders, etc.

The predagonal state is characterized by a darkened, confused consciousness, pallor of the skin, pronounced acrocyanosis, and circulatory disorders. Eye reflexes are preserved, breathing is weakened, the pulse is thready, blood pressure is not determined. Oxygen starvation and acidosis. In the brain tissue, the amount of free sugar decreases, the content of lactic acid increases. Further development of the pathological process leads to agony.

Agony - consciousness is absent, areflexia, sharp pallor of the skin, pronounced cyanosis. The pulse is only on the carotid arteries, the heart sounds are deaf, bradycardia, breathing is arrhythmic, convulsive. Increasing acidosis, oxygen starvation of vital centers.

clinical death. Respiration and cardiac activity are absent. Exchange processes are kept at the lowest level. The vital activity of the organism is minimal. Clinical death lasts 5-6 minutes (V. A. Negovsky, 1969), but the body can still be revived. First of all, the cerebral cortex dies, as a younger (phylogenetically) formation. Subcortical formations are more resistant and viable.

Biological death develops if measures were not taken in time to revive the body. Irreversible processes develop. The use of revitalization methods are useless.

A comprehensive technique for resuscitation of terminal conditions provides for:

Intra-arterial blood injection;

Heart massage (direct and indirect);

defibrillation of the heart;

Artificial ventilation of the lungs;

Auxiliary artificial circulation.

These activities can be carried out simultaneously, or maybe selectively. It is important to know that if clinical death has occurred, then a complex of therapeutic measures can lead to the revival of the body.

Acute respiratory failure (ARF)- a syndrome based on disturbances in the external respiration system, in which the normal gas composition of arterial blood is not ensured or its maintenance at a normal level is achieved due to excessive functional stress of this system.

Etiology.

Distinguish between pulmonary and extrapulmonary causes of ARF.

Extrapulmonary causes:

1. Violation of the central regulation of respiration: a) acute vascular disorders (acute disorders of cerebral circulation, cerebral edema); b) brain injury; c) intoxication with drugs acting on the respiratory center (narcotic drugs, barbiturates); d) infectious, inflammatory and tumor processes leading to damage to the brain stem; e) coma.

2. Damage to the musculoskeletal apparatus of the chest and damage to the pleura: a) peripheral and central paralysis of the respiratory muscles; b) spontaneous pneumothorax; c) degenerative-dystrophic changes in the respiratory muscles; d) poliomyelitis, tetanus; e) spinal cord injury; f) the consequences of the action of organophosphorus compounds and muscle relaxants.

3.ODN in violation of oxygen transport with large blood loss, acute circulatory failure and poisoning (carbon monoxide).

Pulmonary causes:

1. Obstructive disorders: a) blockage of the respiratory tract by a foreign body, sputum, vomit; b) a mechanical obstruction to the access of air when compressed from the outside (hanging, suffocation); c) allergic laringo - and bronchospasm; d) tumor processes of the respiratory tract; e) violation of the act of swallowing, paralysis of the tongue with its retraction; e) edematous-inflammatory diseases of the bronchial tree.

2. Respiratory disorders: a) infiltration, destruction, degeneration of lung tissue; b) pneumosclerosis.

3. Decreased functioning lung parenchyma: a) lung underdevelopment; b) compression and atelectasis of the lung; c) a large amount of fluid in the pleural cavity; d) pulmonary embolism (PE).

ODN classification.

1. Etiological:

Primary ORF - associated with impaired oxygen delivery to the alveoli.

Secondary ARF - associated with a violation of oxygen transport from the alveoli to the tissues.

Mixed ARF - a combination of arterial hypoxemia with hypercapnia.

2.Pathogenetic:

The ventilatory form of ARF occurs when the respiratory center of any etiology is affected, when the transmission of impulses in the neuromuscular apparatus is disturbed, damage to the chest and lungs, changes in the normal mechanics of breathing in the pathology of the abdominal organs (for example, intestinal paresis).

The parenchymal form of ARF occurs with obstruction, restriction of the airways, as well as in violation of the diffusion of gases and blood flow in the lungs.

The pathogenesis of ARF is due to the development of oxygen starvation of the body as a result of violations of alveolar ventilation, diffusion of gases through the alveolar-capillary membranes and uniform distribution of oxygen throughout organs and systems.

There are three main syndromes of ARF:

I. Hypoxia is a condition that develops as a result of reduced tissue oxygenation.

Taking into account etiological factors, hypoxic conditions are divided into 2 groups:

A). Hypoxia due to a reduced partial pressure of oxygen in the inhaled air (exogenous hypoxia), for example, in high altitude conditions.

B) Hypoxia in pathological processes that disrupt the supply of oxygen to tissues at its normal partial voltage in the inhaled air:

Respiratory (respiratory) hypoxia - based on alveolar hypoventilation (impaired airway patency, chest trauma, inflammation and pulmonary edema, respiratory depression of central origin).

Circulatory hypoxia occurs against the background of acute or chronic circulatory failure.

Tissue hypoxia - a violation of the processes of oxygen uptake at the tissue level (potassium cyanide poisoning)

Hemic hypoxia - is based on a significant decrease in erythrocyte mass or a decrease in hemoglobin content in erythrocytes (acute blood loss, anemia).

II. Hypoxemia - a violation of the processes of oxygenation of arterial blood in the lungs. This syndrome can occur as a result of hypoventilation of the alveoli of any etiology (for example, asphyxia), with the predominance of blood flow in the lungs over ventilation with airway obstruction, with impaired diffusion capacity of the alveolar-capillary membrane in respiratory distress syndrome. An integral indicator of hypoxemia is the level of partial oxygen tension in arterial blood (PaO2 is normally 80-100 mm Hg).

III. Hypercapnia - a pathological syndrome characterized by an increased content of carbon dioxide in the blood or at the end of exhalation in the exhaled air. Excessive accumulation of carbon dioxide in the body disrupts the dissociation of oxyhemoglobin, causing hypercatecholaminemia. Carbon dioxide is a natural stimulant of the respiratory center, therefore, at the initial stages, hypercapnia is accompanied by tachypnea, but as it accumulates excessively in the arterial blood, depression of the respiratory center develops. Clinically, this is manifested by bradypnea and respiratory rhythm disturbances, tachycardia, increased bronchial secretion and blood pressure (BP). In the absence of proper treatment, a coma develops. An integral indicator of hypercapnia is the level of partial tension of carbon dioxide in arterial blood (PaCO2 is normally 35-45 mm Hg).

clinical picture.

Shortness of breath, violation of the rhythm of breathing: tachypne, accompanied by a feeling of lack of air with the participation of auxiliary muscles in the act of breathing, with an increase in hypoxia - bradypnoe, Cheyne-Stokes, Biot breathing, with the development of acidosis - Kussmaul breathing.

Cyanosis: acrocyanosis against the background of pallor of the skin and their normal moisture, with increasing cyanosis becomes diffuse, there may be “red” cyanosis against the background of increased sweating (evidence of hypercapnia), “marbling” of the skin, patchy cyanosis.

In the clinic, there are three stages of ARF.

I stage. The patient is conscious, restless, may be euphoric. Complaints about feeling short of breath. The skin is pale, moist, mild acrocyanosis. The number of breaths (RR) is 25-30 per minute, the number of heartbeats (HR) is 100-110 beats / min, blood pressure is within normal limits or slightly increased, PaO2 is 70 mm Hg, PaCO2 is 35 mm Hg. (hypocapnia is compensatory in nature, as a result of shortness of breath).

II stage. Complaints of severe suffocation. Psychomotor agitation. Delusions, hallucinations, loss of consciousness are possible. The skin is cyanotic, sometimes in combination with hyperemia, profuse sweat. Respiratory rate - 30 - 40 per minute, heart rate - 120-140 beats / min, arterial hypertension. PaO2 decreases to 60 mm Hg, PaCO2 increases to 50 mm Hg.

III stage. Consciousness is absent. Seizures. Expansion of pupils with the absence of their reaction to light, spotty cyanosis. Bradypnoe (RR - 8-10 per minute). Falling BP. Heart rate more than 140 beats / min, arrhythmias. PaO2 decreases to 50 mm Hg, PaCO2 increases to 80 - 90 mm Hg. and more.

Acute heart failure (AHF) is a clinical syndrome resulting from a primary heart disease or other diseases in which the heart does not provide sufficient blood circulation to organs and tissues in accordance with their metabolic needs.

OSN classification.

1. Acute left ventricular failure:

Interstitial pulmonary edema or cardiac asthma:

Alveolar pulmonary edema.

Acute right ventricular failure.

Acute biventricular insufficiency.

According to the severity, the following stages of AHF are distinguished (Killip classification):

Stage I - no signs of heart failure.

Stage II - mild AHF: there is shortness of breath, moist fine bubbling rales are heard in the lower parts of the lungs.

Stage III - severe AHF: severe shortness of breath, a significant amount of moist rales over the lungs.

Stage IV - a sharp fall in blood pressure (systolic blood pressure less than 90 mm Hg) up to the development of cardiogenic shock. Severe cyanosis, cold skin, clammy sweat, oliguria, blackout.

Etiology of acute left ventricular heart failure:

1. IHD: acute coronary syndrome (protracted anginal attack, painless widespread myocardial ischemia), acute myocardial infarction (AMI).

2. Mitral valve insufficiency caused by detachment of the papillary muscle (with AMI) or detachment of the mitral valve chord (with infective endocarditis or chest trauma).

3. Stenosis of the left atrioventricular orifice associated with a tumor in any of the chambers of the heart (most often - left atrial myxoma), thrombosis of the mitral valve prosthesis, mitral valve damage in infective endocarditis.

4. Insufficiency of the aortic valve in case of rupture of the aortic valves, with exfoliating aneurysm of the ascending aorta.

5. Acutely increased heart failure in patients suffering from chronic heart failure (acquired or congenital heart defects, cardiomyopathy, post-infarction or atherosclerotic cardiosclerosis); this may be due to hypertensive crisis, paroxysmal arrhythmias, fluid volume overload resulting from inadequate diuretic or excessive fluid therapy.

Etiology of acute right ventricular heart failure:

1.AMI of the right ventricle.

2. Pulmonary embolism (PE).

3. Stenosing process in the right atrioventricular orifice (as a result of a tumor or vegetative growths in infective endocarditis of the tricuspid valve).

4.Asthmatic status.

Etiology of acute biventricular heart failure:

1.AMI with damage to the right and left ventricles.

2. Rupture of the interventricular septum in AMI.

3. Paroxysmal tachycardia.

4. Acute severe myocarditis.

Pathogenesis. Main development mechanisms:

Primary myocardial damage, leading to a decrease in myocardial contractility (CHD, myocarditis).

Pressure overload of the left ventricle (arterial hypertension, aortic valve stenosis).

Left ventricular volume overload (aortic and mitral valve insufficiency, ventricular septal defect).

Decreased filling of the ventricles of the heart (cardiomyopathy, hypertension, pericarditis).

High cardiac output (thyrotoxicosis, severe anemia, cirrhosis of the liver).

Acute left ventricular heart failure.

The main pathogenetic factor is a decrease in the contractility of the left ventricle with preserved or increased venous return, which leads to an increase in hydrostatic pressure in the pulmonary circulation system. With an increase in hydrostatic pressure in the pulmonary capillaries more than 25 - 30 mm Hg. there is an extravasation of the liquid part of the blood into the interstitial space of the lung tissue, which causes the development of interstitial edema. One of the important pathogenetic mechanisms is the foaming of the fluid that has entered the alveoli with each breath, which rises up, filling the bronchi of a larger caliber, i.e. alveolar pulmonary edema develops. So, from 100 ml of sweated plasma, 1 - 1.5 liters of foam is formed. Foam not only disrupts the airway, but also destroys the surfactant of the alveoli, which causes a decrease in lung compliance, increases hypoxia and edema.

Clinical picture:

Cardiac asthma (interstitial pulmonary edema) most often develops at night with a feeling of lack of air, dry cough. The patient is in a forced orthopnea position. Cyanosis and pallor of the skin, cold clammy sweat. Tachypnea, moist rales in the lower parts of the lungs, muffled heart sounds, tachycardia, accent of the second tone over the pulmonary artery.

Alveolar pulmonary edema is characterized by the development of a sharp attack of suffocation, a cough appears with the release of foamy pink sputum, "gurgling" in the chest, acrocyanosis, profuse sweating, tachypnea. In the lungs, mixed moist rales. Tachycardia, accent of the second tone over the pulmonary artery.

Acute right ventricular heart failure is the result of a sharp increase in pressure in the pulmonary artery system. Given the low prevalence of isolated right ventricular AMI and infectious lesions of the tricuspid valve, as a rule, in clinical practice, acute right ventricular failure occurs in combination with left ventricular failure.

Clinical picture: gray cyanosis, tachypnea, acute enlargement of the liver, pain in the right hypochondrium, swelling of the jugular veins, peripheral and abdominal edema.

Acute biventricular heart failure: symptoms of left and right ventricular failure appear simultaneously.

Acute renal failure (ARF) - pathological clinical syndrome of various etiologies, characterized by a significant and rapid decrease in glomerular filtration rate (GFR), which is based on acute damage to the nephron, followed by a violation of its main functions (urinary and urinary) and the occurrence of azotemia, a violation of the acid-base state and water-electrolyte metabolism .

Classification opn.

1. According to the place of occurrence of "damage":

prerenal;

Renal;

Postrenal.

2. By etiology:

Shock kidney - traumatic, hemorrhagic, blood transfusion, septic, anaphylactic, cardiogenic, burn, surgical shock, electrical injury, abortion, postpartum sepsis, severe preeclampsia, dehydration;

Toxic kidney - poisoning with exogenous poisons;

severe infections;

Acute obstruction of the urinary tract;

arenal state.

3.Downstream:

Initial period (period of initial action of factors);

The period of oligo-, anuria (uremia);

Diuresis recovery period:

phase of initial diuresis (diuresis 500 ml/day);

phase of polyuria (diuresis more than 1800 ml / day);

recovery period.

4. By severity:

Grade I - mild: an increase in blood creatinine by 2-3 times;

II degree - moderate: blood creatinine increased by 4-5 times;

Grade III - severe: blood creatinine increased by more than 6 times.

Reasons for the development of the prerenal form of acute renal failure.

1. Decreased cardiac output:

Cardiogenic shock;

Tamponade of the pericardium;

arrhythmias;

Congestive heart failure.

2. Decreased vascular tone:

Anaphylactic, septic shock;

Irrational intake of antihypertensive drugs.

3. Decreased extracellular fluid volume:

bleeding, dehydration,

Profuse vomiting, diarrhea, polyuria.

Reasons for the development of the renal form of acute renal failure.

1. Acute tubular necrosis:

Ischemic;

nephrotoxic;

Drug.

2. Intratubular obstruction:

Pathological cylinders, pigments;

Crystals.

3. Acute tubulointerstitial nephritis:

Drug;

Infectious;

Acute pyelonephritis.

4. Cortical necrosis:

Obstetric;

Anaphylactic shock;

5. Glomerulonephritis.

6. Damage to the renal vessels:

traumatic;

Immunoinflammatory.

Reasons for the development of the postrenal form of acute renal failure.

1. Damage to the ureters:

obstruction (stone, blood clots);

Compression (swelling).

2. Damage to the bladder:

Stones, tumor, inflammatory obstruction, prostate adenoma;

Violation of the innervation of the bladder; spinal cord injury.

3. Urethral stricture.

The pathogenesis is based on a violation of systemic hemodynamics and depletion of the vascular bed of the kidneys. Vasoconstriction is induced with redistribution of blood flow, ischemia of the cortical layer of the kidneys and a decrease in glomerular filtration. The renin - angiotensin - aldosterone system, the production of ADH and catecholamines are activated, which leads to renal vasoconstriction, a further decrease in glomerular filtration, sodium and water retention. If the violation of the blood supply to the kidneys lasts no more than 1-2 hours, their morphological structure is not significantly damaged and functional changes are of a coming nature. If renal blood flow is not restored within 1-2 hours, severe morphological changes form in the kidneys. Clinically, this is manifested by a decrease in diuresis (less than 25 ml / hour) and inhibition of the concentration ability of the kidneys (urine density decreases to 1005 - 1008). After 10-12 hours, azotemia and hyperkalemia increase in the blood plasma.

Symptoms of severe hyperkalemia:

Arrhythmias, bradycardia, AV blockade;

paresthesia;

Muscular paralysis;

Oppression of consciousness.

Symptoms of overhydration quickly join oliguria, and especially anuria - peripheral and abdominal edema, pulmonary edema, cerebral edema. The appearance of an excess of underoxidized products in the body contributes to the development of metabolic acidosis, which at the initial stages of the disease is compensated by respiratory alkalosis (shortness of breath). The accumulation of urea and creatinine in conditions of increased protein catabolism and disturbances in the water and electrolyte state increase metabolic acidosis (vomiting). AKI is characterized by hyperphosphatemia with hypocalcemia. In the polyuric phase, hypocalcemia can cause seizures. Severe intoxication is formed, manifested by headache, irritability, anxiety, and then depression of consciousness of varying severity. As acute renal failure progresses, anemia develops, which may be due to blood loss (hemorrhagic syndrome against the background of uremia), shortened life spans and hemolysis of erythrocytes, as well as a decrease in the production of erythropoietin by the kidneys. Significant suppression of the immune system contributes to the rapid addition of infectious complications.

2. Shock. Pathogenesis, clinical picture, diagnosis.

In shock, the functions of the cardiovascular system, respiration, kidneys change, the processes of microcirculation and metabolism are disturbed. Shock is a polyetiological disease.

In the development of traumatic shock, the main pathogenetic factors are the pain factor and blood loss (plasma loss), which lead to acute vascular insufficiency with microcirculation disorders and the development of tissue hypoxia.

At the heart of hemorrhagic shock is a decrease in the volume of circulating blood and, as a result, a circulatory disorder. A feature of the pathogenesis of septic shock is that circulatory disorders under the influence of bacterial toxins lead to the opening of arteriovenous shunts, and blood bypasses the capillary bed, rushing from arterioles to venules. Cell nutrition is disturbed due to a decrease in capillary blood flow and the action of bacterial toxins directly on the cell, the supply of the latter with oxygen is reduced.

1. Burn shock, its features, shock treatment.

Lasts 1-3 days

Occurs with deep burns of more than 15-20% of the body surface.

Consists of 2 phases: erectile and torpid

Erectile phase - the patient is excited, groans, actively complains of pain, A / D is normal or increased.

Torpid phase - lethargy with preserved consciousness, A / D - a tendency to hypotension, reduced CVP, BCC, diuresis. T body N.

The end of the shock period is indicated by the restoration of diuresis.

Septic shock is a state of peripheral vascular collapse caused by endotoxins from Gram-negative, less commonly Gram-positive bacteria.

Clinic. preceded by a progressive bacterial infection; begins with a sharp increase in body temperature to 3940 ° C, chills; intense sweating; shortness of breath, detoxification; a sharp decrease in blood pressure, up to collapse and loss of consciousness.

A syndrome of multiple organ failure develops: cardiovascular disorders: rhythm disturbance, myocardial ischemia, arterial hypotension; respiratory disorders: tachypnea, hypoxia, respiratory distress syndrome; neuropsychiatric disorders: agitation, convulsions, stupor, coma; impaired renal function: oliguria, hyperazotemia, hypercreatininemia; impaired kidney function: jaundice, increased plasma enzyme activity; hemogram changes: thrombocytopenia, anemia, leukocytosis, leukopenia, hypoproteinemia, acidosis; pronounced changes in the hemostasis system - the development of DIC.

There are 3 phases in the development of septic shock: Phase I - early, "warm": fever up to 3840º C, chills; tachycardia; decrease in systolic blood pressure (SAS) to 9585 mm Hg; decrease in diuresis to 30 ml/hour; duration of the phase several hours and depends on the severity of the infection. Phase II - late or "cold": subnormal body temperature; skin is cold, wet; hemorrhages; severe arterial hypotension (CAC decreases to 70 mm Hg); acrocyanosis, tachycardia, thready pulse; impaired skin sensitivity; oliguria, anuria. Phase III - irreversible septic shock: drop in blood pressure; anuria; coma; RDS

Hemotransfusion shock develops only when incompatible blood is transfused through the AB0, Rhesus systems or other acquired systems. With the complete and high-quality conduct of all tests for compatibility, this complication in the practice of a doctor should not be!

Hemotransfusion shock develops only with "negligent attitude to duties" (Art. 172 of the Code of Criminal Procedure of the Russian Federation). Patients with such complications rarely die immediately, so there is always the possibility of saving them. If you conceal an incompatible blood transfusion with a fatal outcome, you will be held criminally liable under Article 103 of the Code of Criminal Procedure of the Russian Federation, and perhaps, by a court decision, and on charges of a more serious CRIME.

Therapeutic measures for transfusion shock should be aimed at: stopping anaphylaxis, cardiovascular insufficiency, eliminating hypovolemia, but the main task is to restore renal blood flow and diuresis, tk. the maximum burden falls on the kidneys to remove the products of hemolysis of erythrocytes, which clog the renal tubules and form renal failure with the development of anuria. They are carried out in the following order

3. First aid for shock. Complex therapy of shock.

In shock, first aid is more effective the sooner it is given. It should be aimed at eliminating the causes of shock (relieving or reducing pain, stopping bleeding, taking measures to improve breathing and cardiac activity and prevent general cooling).

Pain reduction is achieved by giving the patient or injured limb a position in which there are fewer conditions for intensifying pain, by the behavior of reliable immobilization of the injured part of the body, and by giving painkillers.

In case of injury, the bleeding is stopped and the wound is bandaged; in case of bone fractures and extensive damage to soft tissues, splints are applied. The victim must be treated with the utmost respect.

To facilitate breathing, clothes are unbuttoned (unbutton the collar, loosen the belt).

The patient is laid on his back, his head is somewhat lowered, his legs are raised up by 20-30 cm. In this case, the blood flows towards the heart. At the same time, the volume of circulating blood also increases.

To protect against cooling, the patient is covered with blankets: he must not lose his body heat; other means of keeping warm are unacceptable due to the risk of even greater expansion of blood vessels.

In a state of shock, the patient becomes agitated, he is tormented by fear, so the person providing assistance must constantly be there, reassure and do everything to make the patient feel safe. It is extremely important to protect the patient from noise, for example, conversations of other people.

SHOCK TREATMENT

one . Establish an open airway, intubate and mechanically ventilate if necessary.

2. Position patient with legs elevated effectively for hypotension, especially if no medical equipment is available, however, may impair ventilation and, in cardiogenic shock with pulmonary congestion, also cardiac function.

3 . Place intravascular catheters:

1) to peripheral veins 2 large diameter catheters (better ≥ 1.8 mm [≤ 16 G]), which will allow effective infusion therapy → see below;

2) if necessary, the introduction of many drugs (including catecholamines → see. Below) a catheter into the vena cava; also allows you to monitor central venous pressure (CVP);

3) an arterial catheter (usually a radiation catheter) makes invasive blood pressure monitoring in case of persistent shock or the need for long-term use of catecholamines. Catheterization of the vena cava and arteries should not delay treatment.

4 . Apply etiologic treatment → see below and maintain circulatory system and tissue oxygenation at the same time

1) if the patient is receiving antihypertensive drugs → cancel them;

2) in most types of shock, restoration of intravascular volume by intravenous infusion of solutions is of primary importance; the exception is cardiogenic shock with symptoms of blood stasis in the pulmonary circulation. Colloidal solutions (6% or 10% hydroxyethyl starch [HES], 4% gelatin solution, dextran, albumin solution) have not been shown to be more effective at reducing mortality than crystalloid solutions (Ringer's solution, polyelectrolyte solution, 0.9% NaCl), although to correct hypovolemia, a smaller volume of colloid is needed than crystalloids. Initially, 1000 ml of crystalloids or 300-500 ml of colloids are usually administered over 30 minutes, and this strategy is repeated depending on the effect on blood pressure, CVP and urine output, as well as side effects (symptoms of volume overload). For massive infusions, do not apply 0.9% NaCl alone, as infusion of large volumes of this solution (incorrectly called saline) results in hyperchloremic acidosis, hypernatremia, and hyperosmolarity. Even with hypernatremia, do not apply 5% glucose to restore volemic shock. Colloidal solutions reproduce the intravascular volume - almost completely remain in the vessels (plasma substitutes - gelatin, 5% albumin solution), or remain in the vessels and lead to the transition of water from the extravascular space to the intravascular [plasma volume increasing agents - hydroxyethyl starch [HES], 20% albumin solution, dextrans); solutions of crystalloids equalize the deficit of extracellular fluid (outside and intravascular); glucose solutions increase the volume of total water in the body (external and intracellular fluid). Correction of a significant deficiency of volemia can begin with the infusion of hypertonic solutions, for example, Special mixtures of crystalloids and colloids (so-called. .5% NaCl with 10% HES) as they increase plasma volume better. In patients with severe sepsis or burdened with an increased risk of acute kidney injury, it is better not to use HES especially with a molecular weight ≥ 200 kD and/or a molar substitution > 0.4, an albumin solution can be used instead (however not in patients after a head injury);

3) if hypotension fails despite fluid infusion → start continuous IV infusion (preferably via vena cava catheter) of vasoconstrictor catecholamines, norepinephrine (adrenore, norepinephrine tartrate Agetane), usually 1-20 mcg/min (more than 1-2 mcg / kg / min) or adrenaline 0.05-0.5 mcg / kg / min, or dopamine (dopamine Admeda, Dopamine-Darnitsa, Dopamine hydrochloride, dopamine-Health, Dopmin, currently not drug of choice for septic shock) 3-30 mcg/kg/min and apply invasive blood pressure monitoring. For anaphylactic shock, start with an injection of epinephrine 0.5 mg IM into the outer thigh;

4) in patients with low cardiac output despite appropriate flooding (or in overhydration), administer dobutamine (dobutamine Admeda, dobutamine-Zdorovye) 2-20 mcg/kg/min as a continuous intravenous infusion; if hypotension coexists, a vasoconstrictor drug may be used concomitantly;

5) simultaneously with the treatment described above, use oxygen therapy (maximum oxygenation of hemoglobin increases its supply to tissues; the absolute indication is SaO 2<95%);

6) if, despite the above actions, SvO 2<70%, а гематокрит <30% → примените трансфузию эритроцитарной массы.

5 . The main method of correction of lactic acidosis is etiological treatment and treatment that supports the function of the circulatory system; evaluate the indications for the administration of NaHCO 3 i.v. at pH<7,15 (7,20) или концентрации гидрокарбонатного иона <14 ммоль / л.

6. Monitor vital signs (blood pressure, pulse, respiration), state of consciousness, ECG, SaO 2 , CVP, gasometric parameters (and possibly lactate concentration), natremia and potassium, kidney and liver function parameters; if necessary, cardiac output and wedge pressure in the capillaries of the lungs.

7. Protect the patient from loss of heat and provide the patient with a calm environment.

8. If shock is present:

1) allow bleeding from the gastrointestinal tract and thromboembolic complications (in patients with active bleeding or a high risk of its occurrence, do not use anticoagulant drugs, only mechanical methods);

2) correct hyperglycemia if > 10-11.1 mmol/l) by continuous IV infusion of short-acting insulin, however avoid hypoglycemia; try to keep the glycemic level between 6.7-7.8 mmol/l (120-140 mg/dl) to 10-11.1 mmol/l (180-200 mg/dl).

4. Fainting, collapse, shock. Anti-shock measures.

Fainting is an attack of short-term loss of consciousness due to a temporary violation of cerebral blood flow.

Collapse (from Latin collapsus - fallen) is a life-threatening condition characterized by a drop in blood pressure and a deterioration in the blood supply to vital organs. In humans, it manifests itself as a sharp weakness, pointed facial features, pallor, cold extremities. It occurs with infectious diseases, poisoning, large blood loss, overdose, side effects of certain drugs, etc.

Shock is an acute critical state of the body with progressive insufficiency of the life support system, due to acute circulatory, microcirculation and tissue hypoxia.

Basic anti-shock measures.

Traumatic shock is the body's response to pain stimuli caused by mechanical, chemical or thermal injury.

The frequency and severity of shock increases significantly during a nuclear war. Especially often it will be observed with combined radiation injuries, since the effect of ionizing radiation on the central nervous system disrupts its regular functions. This, in turn, leads to a disruption in the activity of organs and systems, i.e. to metabolic disorders, a drop in blood pressure, which predisposes to the appearance of shock.

Depending on the reasons that led to the shock, there are:

one). Traumatic shock caused by various injuries,

2). Burn shock that occurs after a burn injury,

3). Operational shock caused by surgery with insufficient anesthesia,

SESSION PLAN #40

date according to the calendar-thematic plan

Groups: Medicine

Discipline: Surgery with the basics of traumatology

Number of hours: 2

Topic of the lesson:

Lesson type: lesson learning new educational material

Type of training session: lecture

The goals of training, development and education: formation of knowledge about the main stages of dying, the procedure for resuscitation; concept of post-resuscitation illness;

formation of knowledge about the etiology, pathogenesis, clinic of traumatic shock, the rules for providing PHC, the principles of treatment and patient care.

Education: on the specified topic.

Development: independent thinking, imagination, memory, attention,students' speech (enrichment of vocabulary words and professional terms)

Upbringing: responsibility for the life and health of a sick person in the process of professional activity.

As a result of mastering the educational material, students should: know the main stages of dying, their clinical symptoms, the procedure for resuscitation; have an idea about postresuscitation illness.

Logistics support of the training session: presentation, situational tasks, tests

STUDY PROCESS

Organizational and educational moment: checking attendance at classes, appearance, availability of protective equipment, clothing, familiarization with the lesson plan;

Student survey

Familiarization with the topic, setting learning goals and objectives

Presentation of new material,v polls(sequence and methods of presentation):

Fixing the material : solution of situational problems, test control

Reflection: self-assessment of the work of students in the classroom;

Homework: pp. 196-200 pp. 385-399

Literature:

1. Kolb L.I., Leonovich S.I., Yaromich I.V. General surgery. - Minsk: Vysh.shk., 2008.

2. Gritsuk I.R. Surgery. - Minsk: New Knowledge LLC, 2004

3. Dmitrieva Z.V., Koshelev A.A., Teplova A.I. Surgery with the basics of resuscitation. - St. Petersburg: Parity, 2002

4. L.I.Kolb, S.I.Leonovich, E.L.Kolb Nursing in Surgery, Minsk, Higher School, 2007

5. Order of the Ministry of Health of the Republic of Belarus No. 109 "Hygienic requirements for the arrangement, equipment and maintenance of healthcare organizations and for the implementation of sanitary-hygienic and anti-epidemic measures to prevent infectious diseases in healthcare organizations.

6. Order of the Ministry of Health of the Republic of Belarus No. 165 "On disinfection, sterilization by healthcare institutions

Teacher: L.G. Lagodich

LECTURE SUMMARY

Lecture topic: General disorders of the body's vital functions in surgery.

Questions:

1. Definition of terminal states. The main stages of dying. Preagonal states, agony. Clinical death, signs.

2. Resuscitation measures in terminal conditions. The order of carrying out resuscitation measures, criteria for effectiveness. Conditions for termination of resuscitation.

3. Post-resuscitation disease. Organization of observation and care of patients. biological death. Declaration of death.

4. Rules for handling a corpse.

1. Definition of terminal states. The main stages of dying. Preagonal states, agony. Clinical death, signs.

Terminal States - pathological conditions based on increasing hypoxia of all tissues (primarily the brain), acidosis and intoxication with metabolic products.

During terminal states, the functions of the cardiovascular system, respiration, central nervous system, kidneys, liver, hormonal system, and metabolism decay. The most significant is the extinction of the functions of the central nervous system. Increasing hypoxia and subsequent anoxia in the cells of the brain (primarily the cerebral cortex) lead to destructive changes in its cells. In principle, these changes are reversible and, when normal tissue oxygen supply is restored, do not lead to life-threatening conditions. But with continued anoxia, they turn into irreversible degenerative changes, which are accompanied by protein hydrolysis and, in the end, their autolysis develops. The tissues of the brain and spinal cord are the least resistant to this; only 4–6 minutes of anoxia are necessary for irreversible changes to occur in the cerebral cortex. The subcortical region and the spinal cord can function somewhat longer. The severity of terminal states and their duration depend on the severity and speed of development of hypoxia and anoxia.

Terminal states include:

Severe shock (grade IV shock)

transcendental coma

Collapse

Preagonal state

Terminal pause

Agony

clinical death

Terminal states in their development have3 stages:

1. Preagonal state;

– Terminal pause (since it does not always happen, it is not included in the classification, but it should still be taken into account);

2. An agonal state;

3. Clinical death.

The main stages of dying. Preagonal states, agony. Clinical death, signs.

Ordinary dying, so to speak, consists of several stages, successively replacing each otherStages of dying:

1. Predagonal state . It is characterized by profound disturbances in the activity of the central nervous system, manifested by lethargy of the victim, low blood pressure, cyanosis, pallor or "marbling" of the skin. This condition can last quite a long time, especially in the context of medical care. Pulse and pressure are low or not detected at all. At this stage it often happens terminal pause. It is manifested by a sudden short-term sharp improvement in consciousness: the patient regains consciousness, may ask for a drink, pressure and pulse are restored. But all this is the remnants of the body's compensatory capabilities gathered together. The pause is short, lasting minutes, after which the next stage begins.

2. The next stage -agony . The last stage of dying, in which the main functions of the organism as a whole are still manifested - respiration, blood circulation and the leading activity of the central nervous system. Agony is characterized by a general disorder of body functions, so the provision of tissues with nutrients, but mainly oxygen, is sharply reduced. Increasing hypoxia leads to a cessation of respiratory and circulatory functions, after which the body passes into the next stage of dying. With powerful destructive effects on the body, the agonal period may be absent (as well as the pre-agonal one) or may not last long; with some types and mechanisms of death, it can stretch for several hours or even more.

3. The next step in the process of dying isclinical death . At this stage, the functions of the body as a whole have already ceased, it is from this moment that it is customary to consider a person dead. However, minimal metabolic processes are preserved in the tissues that support their viability. The stage of clinical death is characterized by the fact that a dead person can still be brought back to life by restarting the mechanisms of respiration and blood circulation. Under normal room conditions, the duration of this period is 6-8 minutes, which is determined by the time during which it is possible to fully restore the functions of the cerebral cortex.

4. biological death - this is the final stage of the dying of the organism as a whole, replacing clinical death. It is characterized by irreversible changes in the central nervous system, gradually spreading to other tissues.

Since the onset of clinical death, post-morbid (post-mortem) changes in the human body begin to develop, which are caused by the cessation of body functions as a biological system. They exist in parallel with ongoing life processes in individual tissues.

2. Resuscitation measures in terminal conditions. The order of carrying out resuscitation measures, criteria for effectiveness. Conditions for termination of resuscitation.

The distinction between clinical death (reversible stage of dying) and biological death (irreversible stage of dying) was decisive for the development of resuscitation - a science that studies the mechanisms of dying and reviving a dying organism. The term "resuscitation" itself was first introduced in 1961 by V. A. Negovsky at the International Congress of Traumatologists in Budapest. Anima - soul, re - reverse action, thus - resuscitation is the forced return of the soul to the body.

The formation of resuscitation in the 1960s and 1970s is considered by many to be a sign of revolutionary changes in medicine. This is due to overcoming the traditional criteria of human death - the cessation of breathing and heartbeat - and reaching the level of acceptance of a new criterion - "brain death".

Methods and technique of IVL. Direct and indirect heart massage. Criteria for the effectiveness of resuscitation.

Artificial respiration (artificial lung ventilation - IVL). Need for artificial respiration occurs when breathing is absent or disturbed to such an extent that it threatens the life of the patient. Artificial respiration is an urgent first aid measure for drowning, suffocation (asphyxia during hanging), electric shock, heat and sunstroke, and some poisoning. In case of clinical death, i.e., in the absence of spontaneous breathing and heartbeat, artificial respiration is carried out simultaneously with a heart massage. The duration of artificial respiration depends on the severity of respiratory disorders, and it should continue until fully spontaneous breathing is restored. If there are obvious signs of death, such as cadaveric spots, artificial respiration should be stopped.

The best method of artificial respiration, of course, is to connect special devices to the patient's airways, which can blow the patient up to 1000-1500 ml of fresh air for each breath. But non-specialists, of course, do not have such devices at hand. The old methods of artificial respiration (Sylvester, Schaeffer, etc.), which are based on various methods of chest compression, turned out to be insufficiently effective, since, firstly, they do not provide the release of the airways from the sunken tongue, and secondly, with with their help, no more than 200-250 ml of air enters the lungs in 1 breath.

Currently, mouth-to-mouth and mouth-to-nose breaths are recognized as the most effective methods of artificial respiration (see figure on the left).

The rescuer forcefully exhales air from his lungs into the lungs of the patient, temporarily becoming a breathing apparatus. Of course, this is not the fresh air with 21% oxygen that we breathe. However, as studies by resuscitators have shown, the air exhaled by a healthy person still contains 16-17% oxygen, which is enough to carry out full-fledged artificial respiration, especially in extreme conditions.

So, if the patient does not have his own respiratory movements, you must immediately begin artificial respiration! If there is any doubt whether the victim is breathing or not, one should, without hesitation, begin to “breathe for him” and not waste precious minutes looking for a mirror, applying it to his mouth, etc.

In order to blow "the air of his exhalation" into the patient's lungs, the rescuer is forced to touch the victim's face with his lips. For hygienic and ethical reasons, the following method can be considered the most rational:

1) take a handkerchief or any other piece of cloth (preferably gauze);

2) bite through (break) a hole in the middle;

3) expand it with your fingers up to 2-3 cm;

4) put a tissue with a hole on the nose or mouth of the patient (depending on the chosen method of I. d.); 5) press your lips tightly against the face of the victim through the tissue, and blow through the hole in this tissue.

Artificial respiration "mouth to mouth:

1. The rescuer stands on the side of the victim's head (preferably on the left). If the patient lies on the floor, you have to kneel.

2. Quickly clears the victim's oropharynx from vomit. If the victim's jaws are tightly compressed, the rescuer pushes them apart, if necessary, using a mouth expander tool.

3. Then, putting one hand on the forehead of the victim, and the other on the back of the head, he overbends (that is, throws back) the patient's head, while the mouth, as a rule, opens. To stabilize this position of the body, it is advisable to place a roller from the victim's clothing under the shoulder blades.

4. The rescuer takes a deep breath, slightly delays his exhalation and, bending down to the victim, completely seals the area of \u200b\u200bhis mouth with his lips, creating, as it were, an air-tight dome over the patient's mouth opening. In this case, the patient's nostrils must be clamped with the thumb and forefinger of the hand lying on his forehead, or covered with his cheek, which is much more difficult to do. Lack of tightness is a common mistake in artificial respiration. In this case, air leakage through the nose or corners of the mouth of the victim nullifies all the efforts of the rescuer.

After sealing, the rescuer makes a quick, strong exhalation, blowing air into the respiratory tract and lungs of the patient. Exhalation should last about 1 s and reach 1-1.5 liters in volume in order to cause sufficient stimulation of the respiratory center. In this case, it is necessary to continuously monitor whether the chest of the victim rises well during artificial inspiration. If the amplitude of such respiratory movements is insufficient, then the volume of air blown is small or the tongue sinks.

After the end of the exhalation, the rescuer unbends and releases the victim's mouth, in no case stopping the overextension of his head, because. otherwise, the tongue will sink and there will be no full-fledged independent exhalation. The exhalation of the patient should last about 2 seconds, in any case, it is better that it be twice as long as the inhalation. In a pause before the next breath, the rescuer needs to take 1-2 small ordinary breaths - exhalation “for himself”. The cycle is repeated first with a frequency of 10-12 per minute.

If a large amount of air enters not into the lungs, but into the stomach, the swelling of the latter will make it difficult to save the patient. Therefore, it is advisable to periodically release his stomach from the air, pressing on the epigastric (pituitary) region.

Artificial respiration "mouth to nose" carried out if the patient's teeth are clenched or there is an injury to the lips or jaws. The rescuer, placing one hand on the forehead of the victim, and the other on his chin, hyperextends his head and at the same time presses his lower jaw to the upper. With the fingers of the hand supporting the chin, he should press the lower lip, thereby sealing the mouth of the victim. After a deep breath, the rescuer covers the victim's nose with his lips, creating the same air-tight dome above him. Then the rescuer makes a strong blowing of air through the nostrils (1-1.5 l), while watching the movement of the chest.

After the end of artificial inhalation, it is necessary to release not only the nose, but also the patient's mouth, the soft palate can prevent air from escaping through the nose, and then there will be no exhalation at all when the mouth is closed! It is necessary with such an exhalation to keep the head overbent (i.e., thrown back), otherwise the sunken tongue will interfere with exhalation. The duration of the exhalation is about 2 s. In a pause, the rescuer takes 1-2 small breaths - exhalations “for himself”.

Artificial respiration should be carried out without interruption for more than 3-4 seconds, until full spontaneous breathing is restored or until a doctor appears and gives other instructions. It is necessary to continuously check the effectiveness of artificial respiration (good inflation of the patient's chest, absence of bloating, gradual pinking of the skin of the face). Constantly make sure that vomit does not appear in the mouth and nasopharynx, and if this happens, before the next breath, a finger wrapped in a cloth should be cleared through the mouth of the victim's airways. As artificial respiration is carried out, the rescuer may feel dizzy due to a lack of carbon dioxide in his body. Therefore, it is better that two rescuers carry out air injection, changing after 2-3 minutes. If this is not possible, then every 2-3 minutes, breaths should be reduced to 4-5 per minute, so that during this period the level of carbon dioxide in the blood and brain rises in the person who performs artificial respiration.

When carrying out artificial respiration in a victim with respiratory arrest, it is necessary to check every minute whether he also had a cardiac arrest. To do this, periodically feel the pulse with two fingers on the neck in the triangle between the windpipe (laryngeal cartilage, which is sometimes called the Adam's apple) and the sternocleidomastoid (sternocleidomastoid) muscle. The rescuer places two fingers on the lateral surface of the laryngeal cartilage, after which he “slips” them into the hollow between the cartilage and the sternocleidomastoid muscle. It is in the depths of this triangle that the carotid artery should pulsate.

If there is no pulsation on the carotid artery, an indirect heart massage should be started immediately, combining it with artificial respiration. If you skip the moment of cardiac arrest and perform only artificial respiration without heart massage for 1-2 minutes, then, as a rule, it will not be possible to save the victim.

IVL with the help of equipment - a special conversation in practical classes.

Features of artificial respiration in children. To restore breathing in children under 1 year of age, artificial ventilation of the lungs is carried out according to the method from mouth to mouth and nose, in children older than 1 year - according to the method from mouth to mouth. Both methods are carried out in the position of the child on the back, for children under 1 year old a low roller (folded blanket) is placed under the back or the upper part of the body is slightly lifted with the hand brought under the back, the child's head is thrown back. The caregiver takes a breath (shallow!), hermetically covers the mouth and nose of the child or (in children over 1 year old) only the mouth, and blows air into the child’s respiratory tract, the volume of which should be the smaller, the younger the child (for example, in a newborn it is equal to 30-40 ml). With a sufficient volume of air blown in and air entering the lungs (and not the stomach), chest movements appear. After completing the blow, you need to make sure that the chest is lowering. Blowing an excessively large volume of air for a child can lead to serious consequences - rupture of the alveoli of the lung tissue and air escaping into the pleural cavity. The frequency of inspirations should correspond to the age-related frequency of respiratory movements, which decreases with age. On average, the respiratory rate in 1 minute is in newborns and children up to 4 months. Life - 40, at 4-6 months. - 40-35, at 7 months. - 2 years old - 35-30, at 2-4 years old - 30-25, at 4-6 years old - about 25, at 6-12 years old - 22-20, at 12-15 years old - 20-18.

Heart massage - a method of resuming and artificially maintaining blood circulation in the body by rhythmic contractions of the heart, contributing to the movement of blood from its cavities to the main vessels. Applied in cases of sudden cessation of cardiac activity.

Indications for cardiac massage are determined primarily by general indications for resuscitation, i.e. in the case when there is at least the slightest chance to restore not only independent cardiac activity, but also all other vital body functions. Carrying out heart massage is not indicated in the absence of blood circulation in the body for a long time (biological death) and with the development of irreversible changes in organs that cannot be replaced later by transplantation. It is not advisable to massage the heart if the patient has injuries of organs that are clearly incompatible with life (primarily the brain); with precisely and in advance established terminal stages of oncological and some other incurable diseases. Cardiac massage is not required, and when suddenly stopped blood circulation can be restored using electrical defibrillation in the first seconds of ventricular fibrillation of the heart, established during monitoring of the patient's heart activity, or by applying a jerky blow to the patient's chest in the area of the projection of the heart in case of sudden and documented on screen of the cardioscope of his asystole.

There are direct (open, transthoracic) heart massage, carried out with one or two hands through the chest incision, and indirect (closed, external) heart massage, carried out by rhythmic chest compressions and heart compressions between the sternum and the spine that are displaced in the anteroposterior direction.

Mechanism of actiondirect cardiac massage lies in the fact that when the heart is compressed, the blood in its cavities enters from the right ventricle into the pulmonary trunk and, while artificial ventilation of the lungs is carried out, is saturated with oxygen in the lungs and returns to the left atrium and left ventricle; From the left ventricle, oxygenated blood enters the systemic circulation, and consequently, to the brain and heart. As a result, the restoration of myocardial energy resources makes it possible to resume the contractility of the heart and its independent activity during circulatory arrest as a result of asystole of the ventricles of the heart, as well as ventricular fibrillation, which is successfully eliminated.

Indirect cardiac massage can be performed both by human hands and with the help of special apparatus-massagers.

Direct heart massage is more often more effective than indirect, because. allows you to directly monitor the state of the heart, feel the tone of the myocardium and timely eliminate its atony by injecting intracardiac solutions of adrenaline or calcium chloride, without damaging the branches of the coronary arteries, since it is possible to visually select the avascular region of the heart. However, with the exception of a few situations (for example, multiple rib fractures, massive blood loss, and the inability to quickly eliminate hypovolemia - an "empty" heart), indirect massage should be preferred, because. To perform a thoracotomy, even in an operating room, certain conditions and time are required, and the time factor in resuscitation is decisive. Chest compressions can be started almost immediately after circulatory arrest is detected and can be performed by any previously trained person.

Controlling circulatory efficiency , created by heart massage, is determined by three signs: - the occurrence of pulsation of the carotid arteries in time with the massage,

constriction of the pupils,

And the emergence of independent breaths.

The effectiveness of indirect heart massage is ensured by the correct choice of the place of application of force to the chest of the victim (the lower half of the sternum immediately above the xiphoid process).

The massager's hands should be correctly positioned (the proximal part of the palm of one hand is placed on the lower half of the sternum, and the palm of the other is placed on the back of the first, perpendicular to its axis; the fingers of the first hand should be slightly raised and not exert pressure on the victim's chest) (see. diagrams on the left). They should be straightened at the elbow joints. The person performing the massage should stand high enough (sometimes on a chair, stool, stand, if the patient is lying on a high bed or on the operating table), as if hanging with his body over the victim and putting pressure on the sternum not only by the force of his hands, but also by the weight of his body. The force of pressing should be sufficient to shift the sternum towards the spine by 4-6 cm. The pace of the massage should be such as to provide at least 60 heart compressions in 1 minute. When resuscitation is carried out by two persons, the massager squeezes the chest 5 times with a frequency of approximately 1 time in 1 s, after which the second assister makes one vigorous and quick exhalation from the mouth to the mouth or nose of the victim. In 1 min, 12 such cycles are carried out. If resuscitation is carried out by one person, then the specified mode of resuscitation becomes impossible; the resuscitator is forced to carry out an indirect heart massage in a more frequent rhythm - approximately 15 heart compressions in 12 seconds, then 2 vigorous blows of air into the lungs are carried out in 3 seconds; 4 such cycles are performed in 1 minute, and as a result, 60 heart contractions and 8 breaths. An indirect heart massage can only be effective when combined with artificial lung ventilation.

Monitoring the effectiveness of chest compressions carried out continuously in the course of its implementation. To do this, lift the upper eyelid of the patient with a finger and monitor the width of the pupil. If during 60-90 s of the heart massage there is no pulsation on the carotid arteries, the pupil does not constrict and respiratory movements (even minimal ones) do not appear, it is necessary to analyze whether the rules for conducting a heart massage are strictly followed, resort to medical elimination of myocardial atony or go (subject to conditions) to direct cardiac massage.

If there are signs of the effectiveness of indirect heart massage, but there is no tendency to restore independent cardiac activity, the presence of ventricular fibrillation of the heart should be assumed, which is clarified using electrocardiography. According to the picture of fibrillation oscillations, the stage of ventricular fibrillation of the heart is determined and indications for defibrillation are established, which should be as early as possible, but not premature.

Non-compliance with the rules for conducting an indirect heart massage can lead to complications such as fracture of the ribs, development of pneumo- and hemothorax, liver rupture, etc.

There are somedifferences in chest compressions in adults, children, and neonates . For children aged 2-10 years, it can be carried out with one hand, for newborns - with two fingers, but at a more frequent rhythm (90 per 1 min in combination with 20 breaths of air into the lungs per 1 min).

3. Post-resuscitation disease. Organization of observation and care of patients. biological death. Declaration of death.

If the resuscitation measures are effective and the patient recovers spontaneous breathing and heart contractions. He enters a periodpost-resuscitation illness.

Post-resuscitation period.

In the post-resuscitation period, several stages are distinguished:

1. The stage of temporary stabilization of functions occurs 10-12 hours after the start of resuscitation and is characterized by the appearance of consciousness, stabilization of respiration, blood circulation, and metabolism. Regardless of the further prognosis, the patient's condition improves.

2. The stage of repeated deterioration of the state begins at the end of the first, beginning of the second day. The general condition of the patient worsens, hypoxia increases due to respiratory failure, hypercoagulation develops, hypovolemia due to plasma loss with increased vascular permeability. Microthrombosis and fat embolism impair microperfusion of internal organs. At this stage, a number of severe syndromes develop, from which a "post-resuscitation illness" is formed and delayed death can occur.

3. Stage of normalization of functions.

biological death. Declaration of death.

biological death (or true death) is an irreversible cessation of physiological processes in cells and tissues. Irreversible termination is usually understood as “irreversible within the framework of modern medical technologies” termination of processes. Over time, the possibilities of medicine for the resuscitation of deceased patients change, as a result of which the border of death is pushed into the future. From the point of view of scientists - supporters of cryonics and nanomedicine, most of the people who are dying now can be revived in the future if their brain structure is preserved now.

TO early signs of biological death cadaveric spotswith localization in sloping places of the body, then there isrigor mortis , then cadaveric relaxation, cadaveric decomposition . Rigor mortis and cadaveric decomposition usually begin with the muscles of the face and upper limbs. The time of appearance and duration of these signs depend on the initial background, temperature and humidity of the environment, the reasons for the development of irreversible changes in the body.

The biological death of the subject does not mean the simultaneous biological death of the tissues and organs that make up his body. The time to death of the tissues that make up the human body is mainly determined by their ability to survive in conditions of hypoxia and anoxia. In different tissues and organs, this ability is different. The shortest lifetime under anoxic conditions is observed in the brain tissue, more precisely, in the cerebral cortex and subcortical structures. The stem sections and the spinal cord have a greater resistance, or rather resistance to anoxia. Other tissues of the human body have this property to a more pronounced degree. Thus, the heart retains its viability for 1.5-2 hours after the onset of biological death. Kidneys, liver and some other organs remain viable for up to 3-4 hours. Muscle tissue, skin and some other tissues may well be viable up to 5-6 hours after the onset of biological death. Bone tissue, being the most inert tissue of the human body, retains its vitality for up to several days. The phenomenon of survivability of organs and tissues of the human body is associated with the possibility of their transplantation, and the earlier after the onset of biological death organs are removed for transplantation, the more viable they are, the greater the likelihood of their successful further functioning in another organism.

2. Clothes are removed from the corpse, placed on a specially designed gurney on the back with knees bent, the eyelids are closed, the lower jaw is tied up, covered with a sheet and taken to the sanitary room of the department for 2 hours (until cadaveric stains appear).

3. Only after that, the nurse writes down on the thigh of the deceased his last name, initials, case history number and the corpse is taken to the morgue.

4. Things and valuables are handed over to the relatives or relatives of the deceased on receipt, according to the inventory drawn up at the time of the patient's death and certified by at least 3 signatures (mesestra, nurse, doctor on duty).

5. All bedding from the bed of the deceased is given for disinfection. The bed, bedside table are wiped with a 5% solution of chloramine B, the bedside vessel is soaked in a 5% solution of chloramine B.

6. During the day, it is not customary to place newly admitted patients on the bed where the patient has recently died.

7. It is necessary to report the death of a patient to the admission department of the hospital, to the relatives of the deceased, and in the absence of relatives, as well as in case of sudden death, the cause of which is not clear enough - to the police department.

Topic 11. Wounds and wound healing. Wound definition and wound symptomatology. Types of wounds. The concept of single, multiple, combined and combined wounds. Phases of the course of the wound process. Types of wound healing. Principles of first aid for wounds. Primary surgical treatment of wounds, its types. Secondary surgical treatment. Wound closure by skin grafting.

Purulent wounds primary and secondary. General and local signs of suppuration of the wound. Treatment of a purulent wound depending on the phase of the course of the wound process. The use of proteolytic enzymes. Additional methods of treatment of purulent wounds.

Topic 12. General disorders of life in a surgical patient. Clinical assessment of the general condition of patients. Types of general disorders of the body in surgical patients: terminal conditions, shock, acute blood loss, acute respiratory failure, acute heart failure, dysfunction of the digestive tract, acute renal failure, hemorheological disorders, endogenous intoxication. Glasgow coma scale.

Types, symptoms and diagnosis of terminal states: pre-agony, agony, clinical death. Signs of biological death. First aid in case of cessation of breathing and circulation. Criteria for the effectiveness of revitalization. Monitor control systems. Indications for termination of cardiopulmonary resuscitation.

Shock - causes, pathogenesis, clinical picture, diagnosis, phases and stages of surgical shock. First aid for shock. Complex therapy of shock. Criteria for success in treating shock. Prevention of operational shock. The concept of shocks of another etiology: hemorrhagic shock, cardiogenic shock, anaphylactic shock, septic shock. Intensive care of the consequences of acute and chronic blood loss. The concept of hypoventilation. Diagnosis of insufficiency of the function of external respiration. Equipment for artificial lung ventilation (IVL). Indications for conducting and conducting IVL. Tracheostomy, tracheostomy care. Diagnosis and intensive therapy of disorders of the motor-evacuation function of the digestive tract. Diagnosis of the main syndromes of violation of the water-electrolyte and acid-base state. Principles of drawing up a corrective program. Intensive therapy of disorders of the coagulation system. Diagnosis and intensive therapy of exogenous intoxications. Parenteral nutrition as a component of intensive care.

Topic 13. Mechanical injury. Fractures and dislocations. The concept of trauma. Types of injuries and classification of injuries. The concept of isolated, multiple, combined and combined injuries. Medical prevention of traumatism. Complications and dangers of injuries: immediate, immediate and late. General principles for the diagnosis of traumatic injuries, first aid and treatment. Nonspecific and specific prevention of infectious complications.

Mechanical trauma. Types of mechanical trauma: closed (subcutaneous) and open (wounds). Closed mechanical injuries of soft tissues: bruises, sprains and ruptures (subcutaneous), concussions and compression, prolonged compression syndrome. First aid and treatment of closed soft tissue injuries.

Types of mechanical damage to tendons, bones and joints. Torn ligaments and tendons. Traumatic dislocations. Joint bruises, Hemarthrosis, First aid and treatment. Bone fractures. Classification. Clinical symptoms of fractures. Fundamentals of X-ray diagnostics of dislocations and fractures. The concept of fracture healing. The process of bone formation. First aid for closed and open fractures. Complications of traumatic fractures: shock, fat embolism, acute blood loss, development of infection and their prevention. First aid for spinal fractures with and without spinal cord injury. First aid "for fractures of the pelvic bones with and without damage to the pelvic organs. Transport immobilization - goals, objectives and principles. Types of transport immobilization. Standard splints. Principles of fracture treatment: reposition, immobilization, surgical treatment. The concept of plaster bandages. Gypsum. The basic rules for applying plaster casts The main types of plaster casts Tools and techniques for removing plaster casts Complications in the treatment of fractures The concept of orthopedics and prosthetics.

The concept of traumatic brain injury, classification. The main dangers of head injuries that pose a threat to the life of patients. Tasks of first aid in case of head injury. Measures for their implementation. Features of transportation of patients.

Types of chest injuries: open, closed, with and without damage to the bone base of the chest, with and without damage to internal organs, unilateral and bilateral. The concept of pneumothorax. Types of pneumothorax: open, closed, valvular (tense) external and internal. First aid and features of transportation for tension pneumothorax, hemoptysis, foreign bodies of the lungs, open and closed injuries of the lungs, heart and main vessels. Features of gunshot wounds of the chest, first aid, transportation of the victim.

Abdominal injuries with and without violation of the integrity of the abdominal wall, abdominal organs and retroperitoneal space. First aid tasks for abdominal trauma. Features of first aid and transportation in case of prolapse of abdominal organs into the wound. Features of gunshot wounds of the abdomen. Complications of traumatic injuries of the abdomen: acute anemia, peritonitis.

Features of medical tactics in outpatient settings.

Topic 14. Thermal, chemical and radiation damage. Electrical injury. Combustiology is a branch of surgery that studies thermal injuries and their consequences.

Burns. Burn classification. Recognition of the depth of burns. Determination of the area of the burn. Prognostic methods for determining the severity of burns.

First aid for burns. Primary surgical treatment of the burn surface: anesthesia, asepsis, surgical technique. Methods of treatment of local treatment of burns.: open, closed, mixed. Skin transplant. Antimicrobial therapy (sulfonamides, antibiotics, sera). Outpatient treatment of burns: indications, contraindications, methods. Restorative and plastic surgery of post-burn cicatricial deformities.

Burn disease: 4 periods of its development and course. General principles of infusion therapy for various periods of burn disease, enteral nutrition and patient care.

Types of radiation burns. Features of first aid for radiation burns. Phases of local manifestations of radiation burns. Treatment of radiation burns (first aid and further treatment).

Cold injury. Types of cold injury: common - freezing and chilling; local - frostbite. Prevention of cold injury in peacetime and wartime. Symptoms of freezing and chills, first aid for them and further treatment.

Classification of frostbite by degrees. Clinical course of frostbite: pre-reactive and reactive periods of the disease.

First aid for frostbite in the pre-reactive period. General and local treatment of frostbite in the reactive period, depending on the degree of damage. 0 "general complex therapy for victims of cold injury. Prevention of tetanus and purulent infection, nutrition and care features.

Electrical injury. The effect of electric current on the human body. The concept of electropathology. Local and general effect of electric current. First aid for electrical injury. Features of further examination and treatment of local and general pathology. Lightning strikes. Local and general manifestations. First aid.

Chemical burns. Exposure to caustic chemicals on fabrics. Features of local manifestation. First aid for chemical burns of the skin, oral cavity, esophagus, stomach. Complications and consequences of burns of the esophagus.

Features of medical tactics in outpatient settings.

Topic 15. Fundamentals of purulent-septic surgery. General questions of surgical infection. The concept of surgical infection. Classification of surgical infection: acute and chronic purulent (aerobic), acute anaerobic, acute and chronic specific. The concept of mixed infection.

Local and general manifestations of purulent-septic diseases. Purulent-resorptive fever. Features of asepsis in purulent-septic surgery. Modern principles of prevention and treatment of purulent diseases. Local non-operative and surgical treatment. General principles of the technique of surgical interventions. Modern methods of treatment of purulent focus and methods of postoperative management. General treatment for purulent diseases: rational antibiotic therapy, immunotherapy, complex infusion therapy, hormone and enzyme therapy, symptomatic therapy.

Acute aerobic surgical infection . main pathogens. Ways of infection. The pathogenesis of purulent inflammation. Stages of development of purulent-inflammatory diseases. Classification of acute purulent diseases. local manifestations.

Chronic aerobic surgical infection. Reasons for development. Features of manifestation. Complications: amyloidosis, wound depletion.

Acute anaerobic surgical infection. The concept of clostridial and non-clostridial anaerobic infection. main pathogens. Conditions and factors contributing to the occurrence of anaerobic gangrene and phlegmon. incubation period. clinical forms. Comprehensive prevention and treatment of clostridial anaerobic infection. The use of hyperbaric oxygen therapy. Prevention of nosocomial spread of anaerobic infection.

Place of non-clostridial anaerobic infection in the general structure of surgical infection. Pathogens. Endogenous anaerobic infection. Frequency of anaerobic non-clostridial infection. The most characteristic clinical signs: local and general. Prevention and treatment (local and general) of anaerobic surgical infection.

Topic 16. Acute purulent nonspecific infection. Purulent surgery of the skin and subcutaneous tissue. Types of purulent skin diseases: acne, ostiofolliculitis, folliculitis, furuncle and furunculosis, carbuncle, hydradenitis, erysipelas, erysipeloid, peri-wound pyoderma. Clinic, features of the course and treatment. Types of purulent-inflammatory diseases of the subcutaneous tissue: abscess, cellulitis, phlegmon. Clinic, diagnostics, local and general treatment. Possible complications. Purulent diseases of the lymphatic and blood vessels.

Purulent surgery of the hand. The concept of panaritium. Types of panaritium. Furuncles and carbuncles of the hand. Purulent tendovaginitis. Purulent inflammation of the palm. Purulent inflammation of the back of the hand. Special types of panaritium. Principles of diagnosis and treatment (local and general). Prevention of purulent diseases of the hand.

Purulent surgery of cellular spaces . Phlegmon of the neck. Axillary and subpectoral phlegmon. Subfascial and intermuscular phlegmon of the extremities. Phlegmon of the foot. Purulent mediastinitis. Purulent processes in the tissue of the retroperitoneal space and pelvis. Purulent paranephritis. Purulent and chronic acute paraproctitis. Causes, symptoms, diagnosis, principles of local and general treatment.

Purulent surgery of glandular organs. Purulent parotitis. Predisposing factors, clinical signs, methods of prevention and treatment.

Acute and chronic purulent mastitis. Symptoms, prevention, treatment of acute lactational postpartum mastitis.

Purulent diseases of other glandular organs (pancreatitis, prostatitis, etc.).

Purulent surgery of serous cavities. Introduction to the etiology, clinical manifestations and principles of treatment of purulent meningitis and brain abscesses. Acute purulent pleurisy and pleural empyema. Pericarditis. Purulent diseases of the lungs: abscess and gangrene of the lung, chronic suppurative diseases of the lungs. General ideas about the causes, symptoms, diagnosis and treatment (conservative and operative).

Purulent diseases of the peritoneum and abdominal organs. Acute peritonitis. Classification. Etiology and pathogenesis. Symptomatology and diagnosis. General disorders in the body in acute peritonitis. Principles of treatment. First aid for acute surgical diseases of the abdominal organs.