Lecture Topic: “Critical disabilities in surgical patients” Clinical assessment of the general condition of patients. KGMU Department of General Surgery critical disorders of life in surgical patients. Clinical manifestations of the main syndromes

Acute respiratory failure– a syndrome based on dysfunction of external respiration, leading to insufficient oxygen supply or retention of CO2 in the body. this condition is characterized by arterial hypoxemia or hypercapnia, or both.

The etiopathogenetic mechanisms of acute respiratory disorders, as well as the manifestation of the syndrome, have many features. Unlike chronic, acute respiratory failure is a decompensated condition in which hypoxemia, hypercapnia rapidly progress, and blood pH decreases. Disturbances in the transport of oxygen and CO2 are accompanied by changes in the functions of cells and organs. Acute respiratory failure is one of the manifestations of a critical condition, in which, even with timely and correct treatment, death is possible.

Clinical forms of acute respiratory failure

Etiology and pathogenesis

Acute respiratory failure occurs when there are disturbances in the chain of regulatory mechanisms, including central regulation of respiration and neuromuscular transmission, leading to changes in alveolar ventilation - one of the main mechanisms of gas exchange. Other factors of pulmonary dysfunction include lesions of the lungs (pulmonary parenchyma, capillaries and alveoli), accompanied by significant gas exchange disorders. It should be added that the “mechanics of breathing”, that is, the work of the lungs as an air pump, can also be impaired, for example, as a result of injury or deformation of the chest, pneumonia and hydrothorax, high position of the diaphragm, weakness of the respiratory muscles and (or) airway obstruction. The lungs are a “target” organ that responds to any changes in metabolism. Mediators of critical conditions pass through the pulmonary filter, causing damage to the ultrastructure of the lung tissue. Pulmonary dysfunction of varying degrees always occurs with severe impacts - trauma, shock or sepsis. Thus, the etiological factors of acute respiratory failure are extremely extensive and varied.

In intensive care practice, there are two types of acute respiratory failure: ventilation (hypercapnic) And parenchymal (hypoxemic).

Ventilatory respiratory failure manifested by a decrease in alveolar ventilation. This form of respiratory failure is accompanied by an increase in CO2 in the blood, respiratory acidosis, and arterial hypoxemia.

Causes of ventilation respiratory failure:

 Suppression of the respiratory center by narcotic, sedative drugs, barbiturates, or in connection with diseases and (or) traumatic brain injury (heart attack, cerebral edema, increased intracranial pressure, after-effects of cerebral anoxia, coma of various etiologies);

 Impaired conduction of nerve impulses to the respiratory muscles (due to traumatic injury to the spinal cord, infection such as polio, peripheral neuritis, or neuromuscular blockade caused by muscle relaxants, myasthenia gravis and other factors);

 Weakness or dysfunction of the respiratory muscles, “fatigue” of the diaphragm is a common cause of acute respiratory failure in patients in intensive care units.

 Impaired breathing can be observed with trauma or deformation of the chest, pneumothorax, pleural effusion, or lack of excursion of the diaphragm.

Ventilation respiratory failure often occurs in the immediate postoperative period. Factors contributing to ventilation failure include obesity, old age, smoking, cachexia, and kyphoscoliosis. The increased formation of CO2 in tissues, observed during hyperthermia, hypermetabolism, mainly with carbohydrate energy supply, is not always compensated by an increased volume of pulmonary ventilation.

Parenchymal respiratory failure is characterized by the development of arterial hypoxemia against the background of reduced, normal or increased CO2 levels in the blood. It develops as a result of damage to the lung tissue, pulmonary edema, severe pneumonia, acid aspiration syndrome and many other reasons and leads to severe hypoxemia. The main pathogenetic links of this form of acute respiratory failure are pulmonary shunt (discharge of blood from right to left), discrepancy between ventilation and blood flow, and disruption of diffusion processes.

Causes of parenchymal respiratory insufficiency:

 Trauma, sepsis, systemic inflammatory reaction (released inflammatory mediators: tumor necrosis factor, proinflammatory cytokines, thromboxane, NO, arachidonic acid metabolites, impaired oxygen transport when pulmonary functional units are damaged by oxygen radicals passing through the pulmonary filter;

 Multiple organ failure syndrome (in these cases, lung damage usually occurs);

 Adult respiratory distress syndrome;

 Severe forms of pneumonia;

 Pulmonary contusion;

 Atelectasis;

 Pulmonary edema (caused by an increase in hydrostatic pressure in the pulmonary capillaries or the permeability of the capillary wall);

 Severe form of bronchial asthma;

 Pulmonary embolism;

 Massive bronchopulmonary aspiration.

The identification of two forms of acute respiratory failure is to a certain extent arbitrary. Often one form turns into another. A combination of both forms is also possible.

Clinical picture Acute respiratory failure may be erased during an external examination of the patient and even absent, but it can also be extremely pronounced.

Ventilatory respiratory failure against the background of coma caused by the action of opiates, sedative drugs, anesthesia, is accompanied by minor signs (miosis, shallow breathing). An increase in Pco2 leads to stimulation of the respiratory center, which will most likely result in an increase in all parameters of external respiration. However, this does not happen when exposed to drugs. If active oxygenation is carried out under these conditions, a further decrease in ventilation volume, even apnea, may occur. With the development of ventilation respiratory failure in a patient with initially clear consciousness, blood pressure increases (often up to 200 mm Hg and above), and brain symptoms appear. Very characteristic symptoms of hypercapnia are significant sweating, bronchial hypersecretion and lethargy. If you help the patient cough and eliminate bronchial obstruction, then lethargy disappears. Hypercapnia is also characterized by oliguria, which is always observed with severe respiratory acidosis.

Decompensation of the condition occurs at the moment when the high level of Pco2 in the blood ceases to stimulate the respiratory center. Signs of decompensation in advanced cases include a sharp decrease in minute ventilation, circulatory disorders and the development of coma, which, with progressive hypercapnia, is CO2 narcosis. Pco2 in this case reaches 100 mmHg, but coma can occur earlier - due to hypoxemia. At this stage, it is necessary to carry out artificial ventilation of the lungs with high FiO2. The development of shock against the background of a coma means the beginning of rapid damage to the cellular structures of the brain, internal organs and tissues.

Parenchymal respiratory failure is often not accompanied by symptoms of respiratory failure, with the exception of changes in arterial blood tests indicating a decrease in Po2. it is characterized by a gradual or rapidly progressive course, mild clinical symptoms and the possibility of death within a short time. Initially, tachycardia develops with moderate arterial hypertension, nonspecific neurological manifestations are possible: inadequacy of thinking, confusion of consciousness and speech, lethargy, and so on. Cyanosis is a relatively subjective factor, observed only in the late stage of acute respiratory failure. And corresponding to a significant decrease in saturation and oxygen tension in arterial blood (SaO2< 80%, Po2 < 50ммHg). Внезапно нарушается сознание и развивается кома (гипоксическая) с отсутствием рефлексов, падением артериального давления, остановкой сердечной деятельности. Продолжительность гипоксемической формы острой дахательной недостаточности может колебаться от нескольких минут (при аспирации, асфиксии, синдроме Мендельсона) до нескольких часов и дней (респираторный дистресс синдром взрослых).

Clinical signs of progressive respiratory failure:

 Breathing disorders (shortness of breath, gradual decrease in tidal and minute breathing volumes, oligopnea, mild cyanosis);

 Increasing neurological symptoms (indifference, aggressiveness, agitation, lethargy, coma);

 Disorders of the cardiovascular system (tachycardia, persistent increase in blood pressure during hypercapnia, decompensation of the cardiovascular system and cardiac arrest).

Clinical signs of acute respiratory failure:

 Acute respiratory failure (oligoproe, tachypnea, bradypnea, apnea, pathological rhythms);

 Progressive respiratory hypoxemia (Po2< 50 мм Hg при дыхании воздухом);

 Progressive hypercapnia (Pco2< 50 мм Hg);

 pH< 7,30.

All these signs are not always detected. The presence of at least two of them allows a diagnosis to be made.

Acute heart failure- This is a sudden onset of muscular failure of the ventricles of the heart. This condition can be aggravated by the dissonance between the decreased functioning of one and the normal function of another part of the heart. Sudden onset of cardiac weakness can be fatal.

The causes of acute cardiac dysfunction are myocardial infarction, diffuse myocarditis, excessive physical activity, intercurrent infection, as well as other pathological conditions in which hypercatecholaminemia, a violation of the ionic composition of the intracellular fluid, conduction disturbances, especially in the atrieventricular system (Morgagni-Edams-Stokes attacks) are observed. ), disturbance of excitability (attacks of paroxysmal tachycardia, paroxysmal flutter and atrial fibrillation and ventricular fibrillation leading to asystole).

Symptoms of acute heart failure

The clinical picture of acute heart failure, accompanied by a drop in cardiac output and a sharp decrease in blood supply to the arterial system, is very reminiscent of the picture of acute vascular circulatory failure, which is why it is sometimes referred to as acute cardiac collapse, or cardiogenic shock. Patients experience extreme weakness, a state close to fainting), pallor, cyanosis, coldness of the extremities, and very low pulse filling. Recognition of acute weakness of the heart is based primarily on the detection of changes in the heart (expansion of the boundaries of the heart, arrhythmia, pre-diastolic gallop rhythm). In this case, shortness of breath, swelling of the neck veins, congestive wheezing in the lungs, and cyanosis are observed. A sharp slowdown (less than 40 per minute) or increased heart rate (more than 160 per minute) is more characteristic of cardiac weakness than vascular weakness. Blood pressure is reduced. There are symptoms of organ ischemia with symptoms of venous congestion due to the disproportion between the total mass of circulating blood and its effective volume.

Acute syndrome right ventricular failure most clearly manifested in cases of blockage of the pulmonary artery trunk or its large branch due to the introduction of a blood clot from the veins of the legs, pelvis, or less often from the right ventricle or atrium. The patient suddenly develops shortness of breath, cyanosis, sweat, a feeling of constriction or pain in the heart area, the pulse becomes very small and frequent, and blood pressure drops. Soon, if the patient remains alive, venous pressure increases, the neck veins swell, and then the liver enlarges, an accent of the second tone on the pulmonary artery and a gallop rhythm are heard. X-ray reveals an enlargement of the right ventricle and expansion of the conus of the pulmonary artery. After 1-2 days, signs of heart attack and pneumonia may appear.

Acute right ventricular failure can be observed in patients with acute myocardial infarction of the posterior wall with concomitant pneumosclerosis and pulmonary emphysema. Along with the clinical picture of myocardial infarction, they experience cyanosis, congestion in the systemic circulation, and sudden enlargement of the liver. Sometimes patients are admitted to the surgical department with a diagnosis of acute abdomen and acute cholecystitis due to severe pain in the right hypochondrium due to stretching of the liver capsule.

Acute left ventricular failure clinically manifested by cardiac asthma and pulmonary edema.

Cardiac asthma is an attack of asthma.

It should be borne in mind that the clinical picture of acute left ventricular failure also develops in cases of mechanical closure of the left atrioventricular orifice by a moving thrombus in mitral stenosis. Characteristic is the disappearance of the arterial pulse along with a noticeable strong heartbeat, the appearance of acute pain in the heart area, shortness of breath, increasing cyanosis with subsequent loss of consciousness and the development in most cases of reflex collapse. Prolonged closure of the atrioventricular orifice by a thrombus usually leads to the death of patients.

Similarly, with mitral stenosis, acute functional failure syndrome of the left atrium is often observed. This happens when the defect is compensated by increased work of the left atrium while the contractile function of the right ventricle is preserved. With excessive physical stress, sudden stagnation of blood in the vessels of the lungs can occur and an attack of cardiac asthma may occur, which can develop into acute pulmonary edema. Sometimes such attacks are repeated frequently, appear suddenly and disappear just as suddenly, which confirms the great importance of the reflex influence from the atria to the pulmonary vessels.

Until now, all the mechanisms of development of cardiac asthma have not been deciphered. Convincing data have been obtained on the role of the central and autonomic nervous systems in the occurrence of these attacks. Hormonal factors also have a big influence.

It is known that attacks of cardiac asthma and pulmonary edema can occur when the cardiac probe irritates the pulmonary artery receptors during cardiac probing.

With physical exertion, excitement, fever, pregnancy, etc., there is an increased need for oxygen in the body, increased cardiac activity and increased cardiac output, which in patients with existing heart lesions can lead to suddenly developing weakness of the left side of the heart. A decompensated difference in the ejection of blood from the right and left parts of the heart leads to overflow of the pulmonary circulation. Pathological reflexes due to hemodynamic disturbances lead to the fact that the production of glucocorticoids decreases, and mineralocorticoids increases. This, in turn, increases vascular permeability and causes sodium and water retention in the body, which further worsens hemodynamic parameters.

It is necessary to take into account one more factor that can play a big role in the development of these complications - a violation of lymph circulation in the lung tissue, expansion of the anastomoses between the veins of the large and small circle.

Long-term increase in capillary pressure in the lungs above 30 mmHg. Art. causes fluid to leak from the capillaries into the alveoli and can lead to pulmonary edema. At the same time, as shown in the experiment, a short-term increase in capillary pressure in the lungs, reaching 50 mm Hg. Art. and more, does not always lead to pulmonary edema. This indicates that capillary pressure is not the only factor influencing the development of pulmonary edema. A significant role in the development of pulmonary edema belongs to the permeability of the alveolar and capillary walls and the degree of precapillary pressure. Thickening and fibrosis of the alveolar wall may prevent the development of pulmonary edema at high capillary pressure. With increased capillary permeability (anoxemia, infections, anaphylactic shock, etc.), pulmonary edema can develop even when the capillary pressure is significantly below 30 mm Hg. Art. Pulmonary edema occurs in patients with a small difference between the pressure in the pulmonary artery and pulmonary capillaries and low pulmonary arteriolar resistance. When the pressure gradient between the pulmonary artery and the pulmonary capillaries is high, there is a high pulmonary arteriolar resistance, which creates a protective barrier that protects the pulmonary capillaries from overflowing with blood, a sharp increase in pressure in them, and, consequently, from the occurrence of cardiac asthma or pulmonary edema . In patients with pronounced narrowing of the left venous ostium, development of muscle fibers in the pulmonary arterioles, proliferation of fibrous tissue in the intima of vessels, thickening of the pulmonary capillaries, hypertrophy of the fibrous base with partial loss of elasticity of the pulmonary tissue were noted. In this regard, the pulmonary capillaries move away from the alveolar membrane, and the alveolar membranes themselves thicken. This restructuring begins when the pressure in the pulmonary artery increases to 50 mm Hg. Art. and higher and is most pronounced in the pulmonary vessels with an increase in pulmonary arterial pressure to 90 mm Hg. Art. and higher.

These changes reduce the permeability of blood vessels and alveolar membranes. However, these morphological changes in patients with mitral stenosis do not exclude the possibility of them developing attacks of suffocation or pulmonary edema. Capillary extravasation is also possible with these changes, but at a higher “critical” level of pulmonary capillary pressure necessary for the occurrence of capillary extravasation and the passage of tissue fluid through the altered alveolar membranes.

Clinic for cardiac asthma and pulmonary edema characterized initially by the occurrence of severe suffocation and severe cyanosis. A large number of scattered dry and moist rales are detected in the lungs. There is bubbling breathing, a cough with the release of foamy sputum (often blood-stained). Blood pressure often decreases.

Acute renal failure (ARF)- this is a sudden, potentially reversible, significant decrease or complete cessation of all (secretory, excretory and filtration) functions of the kidneys. Every second patient with acute renal failure needs hemodialysis. Currently, there is a trend in which acute renal failure is identified as one of the manifestations of multiple organ failure syndrome.

CAUSES

All the reasons that cause the development of acute renal failure can be divided into three large groups:

1. Extrarenal (extrarenal) causes- lead to a decrease in blood volume and a sharp decrease in renal blood flow, which can cause irreversible death of renal tissue cells. Extrarenal causes of acute renal failure include: severe extensive operations, especially in weakened or elderly patients; injuries accompanied by painful shock and hypovolemia; sepsis; massive blood transfusion; extensive burns; uncontrollable vomiting; uncontrolled use of diuretics; cardiac tamponade.

2. Renal (renal) causes– include ischemic and toxic damage to the renal tissue, acute inflammation of the renal parenchyma or damage to the renal vessels, which cause necrosis of the renal tissue. Renal causes of acute renal failure include: acute glomerulonephritis; acute tubular necrosis; rheumatic kidney damage; blood diseases; poisoning with mercury, copper, cadmium salts, poisonous mushrooms, organic fertilizers; malignant arterial hypertension; lupus nephritis; uncontrolled use of drugs from the group of sulfonamides, antitumor drugs, aminoglycosides, NSAIDs.

3. Subrenal (postrenal) causes– are associated with a violation of the outflow of urine, which leads to the accumulation of urine in the collecting system, edema and necrosis of renal tissue cells. Renal causes of acute renal failure include: bilateral obstruction of the ureters by stones or blood clots; urethritis and periurethritis; tumors of the ureters, prostate, bladder; long-term compression of the ureters during trauma, surgical interventions on the abdominal organs.

CLASSIFICATION

Depending on the causes of development, prerenal, renal and postrenal acute renal failure are distinguished, respectively.

SYMPTOMS

With acute renal failure, there is a sharp disruption of all functions performed by the kidneys. The loss of the kidneys' ability to maintain the balance of electrolytes in the blood is accompanied by an increase in the concentration of calcium and potassium ions and chlorine, as well as the accumulation of protein metabolic products and an increase in the level of urea and creatinine in the blood. Violation of the secretory function of the kidneys causes the development of anemia and thrombocytopenia. As a consequence of impaired renal excretory function, one of the main symptoms of acute renal failure develops - oliguria (decreased urine output) up to anuria (complete absence of urine). The condition of patients with acute renal failure is usually moderate or severe, disturbances of consciousness occur (lethargy or excessive agitation), swelling of the extremities, cardiac arrhythmias, nausea and vomiting, and an increase in the size of the liver is determined.

The clinical course of acute renal failure is divided into several stages, successively replacing each other.

1. At the initial stage of acute renal failure, which usually lasts several hours, less often several days, circulatory collapse develops, accompanied by severe ischemia of the renal tissue. The patient's condition may be different; it is determined by the main cause of the development of acute renal failure.

2. At the stage of oligoanuria, there is a sharp reduction in urine volume (no more than 0.5 liters of urine per day) or a complete absence of urination. This stage usually develops within three days from the onset of acute renal failure, but can extend to 5-10 days. Moreover, the later acute renal failure develops and the longer its duration, the worse the prognosis of the disease and the higher the likelihood of death. With prolonged oligoanuria, the patient becomes lethargic and lethargic, and may fall into a coma. Due to pronounced suppression of immunity, the risk of secondary infection with the development of pneumonia, stomatitis, mumps, etc. increases.

3. During the diuretic stage, there is a gradual increase in urine volume, reaching about 5 liters of urine per day. The duration of the diuretic stage is usually 10-14 days, during which a gradual regression of the symptoms of renal failure occurs and the electrolyte balance of the blood is restored.

4. At the recovery stage, further restoration of all kidney functions occurs. It may take 6 months to a year to fully restore kidney function.

Acute liver failure develops as a result of massive necrosis of hepatocytes, which leads to a sharp deterioration in liver function in patients without pre-existing liver disease. The main symptom of acute renal failure is hepatic encephalopathy (HE), which decisively influences the course of acute renal failure and the prognosis of the disease.

We can talk about acute renal failure if encephalopathy develops within 8 weeks from the onset of the first symptoms of acute hepatic cellular failure. If PE develops within 8 to 24 weeks from the onset of the first symptoms of liver damage, then we should talk about subacute liver failure. In addition, it is advisable to distinguish between hyperacute liver failure, which develops within 7 days of the onset of jaundice. Mortality in acute renal failure, according to various authors, ranges from 50 to 90%.

The main etiological factors for the development of acute renal failure are:

1. Viral hepatitis.

2. Drug poisoning (paracetamol).

3. Poisoning with hepatotoxic poisons (mushrooms, alcohol substitutes, etc.).

4. Wilson–Konovalov disease.

5. Acute fatty degeneration of the liver in pregnant women.

Main symptoms and complications of acute renal failure

Hepatic Encephalopathy is a complex of potentially reversible neuropsychiatric disorders that arise as a consequence of acute or chronic liver failure and/or portosystemic blood shunting.

According to most researchers, HE develops due to the penetration of endogenous neurotoxins through the blood-brain barrier (BBB) ​​and their effect on astroglia as a result of liver cell failure. In addition, the amino acid imbalance that occurs in liver failure affects the development of PE. As a result, the permeability of the BBB and the activity of ion channels change, neurotransmission and the supply of neurons with high-energy compounds are disrupted. These changes underlie the clinical manifestations of PE.

Hyperammonemia in liver diseases is associated with a decrease in the synthesis of urea and glutamine in the liver, as well as with portosystemic blood shunting. Ammonia in non-ionized form (1-3% of total blood ammonia) easily penetrates the BBB, stimulating the transport of aromatic amino acids into the brain, resulting in increased synthesis of false neurotransmitters and serotonin.

According to some authors, in addition to ammonia, neurotoxins involved in the pathogenesis of PE include mercaptans, short- and medium-chain fatty acids, and phenols formed from the corresponding substrates under the influence of intestinal bacteria. The mechanisms of their action are similar and are associated with inhibition of neuronal Na+,K+-ATPase and increased transport of aromatic amino acids into the brain. Short- and medium-chain fatty acids, in addition, inhibit the synthesis of urea in the liver, which contributes to hyperammonemia.

Finally, there are indications of the role of the inhibitory neurotransmitter g-aminobutyric acid (GABA) of intestinal origin in the pathogenesis of PE, the excessive supply of which to the brain under conditions of astroglial edema also leads to an increase in neuropsychic disorders characteristic of PE.

It is important to note that a clear relationship between the concentrations of each of the listed metabolites involved in the pathogenesis of PE and the severity of encephalopathy has not been established. Thus, PE appears to be the result of a complex effect and mutual reinforcement of several factors: endogenous neurotoxins, among which ammonia is of leading importance, amino acid imbalance and changes in the functional activity of neurotransmitters and their receptors.

The development of encephalopathy in patients with acute renal failure is dominated by factors of parenchymal liver failure, the outcome of which is often endogenous hepatic coma. Provoking factors in this case are the increased breakdown of proteins contained in the diet, or when blood protein enters during gastrointestinal bleeding, irrational use of medications, alcoholic excesses, surgical interventions, concomitant infections, etc. Encephalopathy in patients with cirrhosis of the liver can be episodic with spontaneous resolution or intermittent, lasting many months or even years. In accordance with the criteria of the International Association for the Study of Liver Diseases (Brighton, UK, 1992) and the standardization of nomenclature, diagnostic signs and prognosis of liver and biliary tract diseases (C. Leevy et al., 1994), latent and clinically pronounced (4 stages) PE are distinguished .

1. General symptoms of acute renal failure: nausea, vomiting, anorexia, hyperthermia, malaise and progressive fatigue.

2. Jaundice is a mirror of the degree of liver failure. Bilirubin levels may increase to 900 µmol/L.

3. “Liver odor” from the mouth (smell of rotten meat).

4. Flopping tremor. Determined in conscious patients. In addition, it can be recorded with uremia, respiratory failure, low levels of potassium in the blood plasma, as well as intoxication with a number of drugs.

5. Ascites and edema (associated with a decrease in albumin levels in the blood).

6. Deficiency of coagulation factors due to a decrease in their production by the liver. The platelet count also decreases. As a result, gastrointestinal bleeding and diapedetic bleeding from the nasopharynx, retroperitoneal space, and injection sites often develop.

7. Metabolic disorders. Typically, hypoglycemia develops as a result of gluconeogenesis and an increase in insulin levels.

8. Cardiovascular complications:

hyperdynamic circulation (reminiscent of septic shock) - increased cardiac index, low peripheral resistance, arterial hypotension;

hypovolemia;

enlarged heart;

pulmonary edema;

arrhythmias (atrial fibrillation and ventricular extrasystoles);

pericarditis, myocarditis and bradycardia develop in the terminal phase of acute liver failure.

9. Sepsis. The septic condition is enhanced by the phenomena of immunological dysfunction. The most common pathogens are Staphylococcus aureus/Streptococci, intestinal flora.

10. Renal failure (hepatorenal syndrome). Most patients with acute renal failure have renal failure, which is manifested by oliguria and increased blood creatinine levels. In cases of acetaminaphen poisoning, renal failure also develops as a result of the direct toxic effect of the drug. Tubular damage can develop as a result of hypotension and hypovolemia. Blood urea levels in acute renal failure are usually low as a result of decreased synthesis in the liver.

Differential diagnosis of acute (fulminant) liver failure should be made with bacterial meningitis, brain abscess, and encephalitis.

CRITICAL DISORDERS IN SURGICAL PATIENTS prof. R.T. Majidov

Comatose states

Glasgow scale (score assessment of the functional state of the central nervous system)

Stages of the breathing process

Lung volumes and capacities

Parenchymal mechanism of pulmonary gas exchange disorder

Ventilation mechanism of pulmonary gas exchange disorder

Types of acute respiratory failure

Indicators of hemodynamic mechanisms

Clinical syndrome of circulatory disorders

Causes of primary cardiac arrest

Cardiac arrest options

Acute cardiac arrest clinic

Forms of circulatory failure

Forms of acute circulatory disorders

Water-electrolyte imbalance syndromes

Syndromes of acid-base balance disorder

Types of shock

Types of critical conditions

Metabolic functions in critical conditions and their correction

Parenteral nutrition

Terminal state

While studying the topic, the student must have the following professional competencies:

Able and willing to identify critical disability in surgical patients

Able and willing to provide first aid for critical life events

I. Motivation for the purpose of the lesson

Knowledge of critical disabilities is necessary not only for the professional activities of a doctor of any specialty, but also in a person’s everyday life, because allows you to master methods of providing timely and targeted assistance in case of an accident in any conditions.

II. The purpose of self-training. To study the clinical signs and principles of medical care for conditions such as acute respiratory failure, acute cardiovascular failure, acute renal and liver failure, multiple organ failure syndrome.

III. Educational-target tasks

After independently studying the material on this topic, the student must

Know:

Ø clinical manifestations of acute respiratory failure;

Ø clinical manifestations of acute heart failure;

Ø clinical manifestations of acute renal failure;

Ø clinical manifestations of acute liver failure;

Ø clinical manifestations of multiple organ failure syndrome.

Be able to:

Ø diagnose acute respiratory failure, acute heart failure, acute renal and liver failure, multiple organ failure syndrome based on clinical symptoms;

Ø diagnose clinical death;

Ø provide first aid for respiratory failure;

Ø provide first aid for heart failure;

Ø provide first aid for renal failure;

Ø provide first aid for liver failure.

Own:

Ø an algorithm for determining the type of critical condition and skills in providing first aid to sick adults and surgical teenagers.

IV. Initial level of knowledge

The student must repeat the concept of first aid, indicators of the state of the functions of vital organs (blood pressure, pulse, frequency and amplitude of respiratory movements, etc.).

V. Topic study plan

1. Clinical assessment of general condition.

2. Types of dysfunction of the body in surgical patients.

3. Causes, development mechanisms, principles of diagnosis and treatment of acute respiratory failure.

4. Causes, development mechanisms, principles of diagnosis and treatment of acute heart failure.

5. Causes, development mechanisms, principles of diagnosis and treatment of acute renal failure.

6. Causes, development mechanisms, principles of diagnosis and treatment of acute liver failure.

7. Causes, development mechanisms, principles of diagnosis and treatment of multiple organ failure syndrome.

1. Sumin, S.A. Emergency conditions: textbook. manual for medical students. universities / S.A. Sumin. 6th ed., revised. and additional - M.: MIA, 2006. - 799 p.: ill. (Educational literature for students of medical universities and departments).

2. Practical skills and abilities in the course “General Surgery”: textbook. a manual for students of all faculties / ed. B.S. Sukovatykh; GOU VPO "Kursk State Medical University", department. general surgery.-Kursk: Publishing house of KSMU, 2009.-175 p.: ill.

3. Multimedia course of lectures on general surgery for self-training of 3rd year students of the Faculty of Medicine Kursk KSMU 2012.

Electronic library of a medical university “Student Consultant” www/studmedib.ru

4. General surgery: textbook / Petrov S.V. - 3rd ed., revised. and additional - M.: GEOTAR-Media, 2010. - 768 p. : ill.

5. General surgery: textbook / Gostishchev V.K. - 4th ed., revised. and additional - M.: GEOTAR-Media, 2010. - 848 p.

VII. Questions for self-control

6. By what criteria is the general condition of the patient assessed?

LESSON PLAN #40

date according to the calendar and thematic plan

Groups: General Medicine

Discipline: Surgery with basics of traumatology

Number of hours: 2

Topic of the training session:

Type of training session: lesson on learning new educational material

Type of training session: lecture

Goals of training, development and education: formation of knowledge about the main stages of dying, the procedure for carrying out resuscitation measures; idea of ​​post-resuscitation illness;

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

Education: on the specified topic.

Development: independent thinking, imagination, memory, attention,student 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 of ​​post-resuscitation illness.

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

PROGRESS OF THE CLASS

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

Student Survey

Introduction to the topic, setting educational goals and objectives

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

Fixing the material : solving situational problems, test control

Reflection: self-assessment of students’ work in class;

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

Literature:

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

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

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 design, equipment and maintenance of healthcare organizations and for the implementation of sanitary, hygienic and anti-epidemic measures for the prevention of infectious diseases in healthcare organizations.

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

Teacher: L.G.Lagodich

LECTURE NOTES

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 for terminal conditions. The procedure for resuscitation measures, effectiveness criteria. Conditions for terminating resuscitation measures.

3. Post-resuscitation illness. Organization of observation and care for patients. Biological death. Ascertainment 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 products of impaired metabolism.

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

Terminal conditions include:

Severe shock (IV degree shock)

Transcendent 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 is still worth taking into account);

2. 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 that successively replace each other.Stages of dying:

1. Preagonal state . It is characterized by profound disturbances in the activity of the central nervous system, manifested by the victim’s lethargy, 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 blood pressure are low or not detected at all. It often happens at this stage terminal pause. It manifests itself as a sudden short-term sharp improvement in consciousness: the patient regains consciousness, may ask for a drink, blood pressure and pulse are restored. But all this is the remnants of the body’s compensatory capabilities put together. The pause is short-lived, lasting minutes, after which the next stage begins.

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

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

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.

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

2. Resuscitation measures for terminal conditions. The procedure for resuscitation measures, effectiveness criteria. Conditions for terminating resuscitation measures.

The distinction between clinical death (the reversible stage of dying) and biological death (the irreversible stage of dying) was decisive for the development of resuscitation - a science that studies the mechanisms of dying and revival of 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 is the soul, re is the reverse action, thus - resuscitation is the forced return of the soul to the body.

The formation of resuscitation in the 60-70s is considered by many to be a sign of revolutionary changes in medicine. This is due to overcoming the traditional criteria of human death - cessation of breathing and heartbeat - and reaching the level of acceptance of a new criterion - “brain death”.

Methods and techniques for performing mechanical ventilation. Direct and indirect cardiac massage. Criteria for the effectiveness of resuscitation measures.

Artificial respiration (artificial pulmonary ventilation - mechanical ventilation). Need for artificial respiration occurs in cases where breathing is absent or impaired to such an extent that it threatens the patient’s life. Artificial respiration is an emergency first aid measure for drowning, suffocation (asphyxia from hanging), electric shock, heat and sunstroke, and some poisonings. In case of clinical death, i.e. in the absence of independent breathing and heartbeat, artificial respiration is carried out simultaneously with cardiac massage. The duration of artificial respiration depends on the severity of respiratory disorders, and it should continue until independent breathing is completely restored. If obvious signs of death, such as cadaveric spots, appear, artificial respiration should be stopped.

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

Currently, the most effective methods of artificial respiration are considered to be mouth-to-mouth and mouth-to-nose blowing (see figure on the left).

The rescuer forcefully exhales air from his lungs into the patient's lungs, 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 artificial respiration, especially in extreme conditions.

So, if the patient does not have his own breathing movements, he must immediately begin artificial respiration! If there is any doubt whether the victim is breathing or not, you must, without hesitation, start “breathing for him” and not waste precious minutes looking for a mirror, putting it to your 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. From hygienic and ethical considerations, the following technique can be considered the most rational:

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

2) bite (tear) a hole in the middle;

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

4) place the fabric with the hole on the patient’s nose or mouth (depending on the chosen method of ID); 5) press your lips tightly to the victim’s face 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 is lying on the floor, you have to kneel.

2. Quickly clears the victim’s oropharynx of vomit. If the victim's jaws are tightly clenched, the rescuer moves them apart, if necessary, using a mouth retractor tool.

3. Then, placing one hand on the victim’s forehead and the other on the back of the head, he hyperextends (that is, tilts 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 cushion from the victim’s clothing under the shoulder blades.

4. The rescuer takes a deep breath, slightly holds his exhalation and, bending over to the victim, completely seals the area of ​​his mouth with his lips, creating, as it were, an air-impermeable dome over the patient’s mouth. In this case, the patient’s nostrils must be closed 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 during artificial respiration. In this case, air leakage through the nose or corners of the victim’s mouth negates all the efforts of the rescuer.

After sealing, the rescuer exhales quickly, forcefully, blowing air into the patient's airways and lungs. The 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 victim’s chest rises well during artificial inhalation. If the amplitude of such respiratory movements is insufficient, it means that the volume of air blown in is small or the tongue sinks.

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

If a large amount of air gets into the stomach, rather than into the lungs, the swelling of the latter will make it difficult to save the patient. Therefore, it is advisable to periodically empty his stomach of air by pressing on the epigastric (epigastric) region.

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

After the end of artificial inhalation, it is necessary to empty not only the nose, but also the patient’s mouth; the soft palate can prevent air from escaping through the nose, and then with the mouth closed, there will be no exhalation at all! During such an exhalation, it is necessary to maintain the head hyperextended (i.e., tilted back), otherwise a sunken tongue will interfere with exhalation. The duration of exhalation is about 2 s. During the pause, the rescuer takes 1-2 small breaths and exhales “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 pinkening of the facial skin). Always make sure that vomit does not appear in the mouth and nasopharynx, and if this happens, before the next inhalation, use a finger wrapped in a cloth to clear the victim’s airways through the mouth. As artificial respiration is carried out, the rescuer may become dizzy due to the lack of carbon dioxide in his body. Therefore, it is better for two rescuers to carry out air injection, changing every 2-3 minutes. If this is not possible, then every 2-3 minutes you should reduce your breaths to 4-5 per minute, so that during this period the level of carbon dioxide in the blood and brain of the person performing artificial respiration rises.

When performing artificial respiration on a victim with respiratory arrest, it is necessary to check every minute whether he has also suffered cardiac arrest. To do this, you need to periodically feel the pulse in the neck with two fingers 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, and then “slides” 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 in the carotid artery, you must immediately begin chest compressions, combining it with artificial respiration. If you skip the moment of cardiac arrest and perform only artificial respiration on the patient without cardiac massage for 1-2 minutes, then, as a rule, it will not be possible to save the victim.

Ventilation using equipment is a special topic in practical classes.

Features of artificial respiration in children. To restore breathing in children under 1 year of age, artificial ventilation is carried out using the mouth-to-mouth and nose method, in children over 1 year of age - using the mouth-to-mouth method. Both methods are carried out with the child in the supine position; for children under 1 year of age, a low cushion (folded blanket) is placed under the back or the upper body is slightly raised with an arm placed under the back, and the child’s head is thrown back. The person providing assistance takes a breath (shallow!), hermetically covers the child’s mouth and nose 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 smaller the younger the child is (for example, in a newborn it is equal to 30-40 ml). When there is a sufficient volume of air blown in and the air enters the lungs (and not the stomach), movements of the chest appear. Having finished insufflation, you need to make sure that the chest descends. Blowing in a volume of air that is too large for a child can lead to serious consequences - rupture of the alveoli of the lung tissue and the release of air into the pleural cavity. The frequency of insufflations should correspond to the age-related frequency of respiratory movements, which decreases with age. On average, the respiratory rate is 1 minute in newborns and children up to 4 months. Life - 40, at 4-6 months. - 40-35, at 7 months. - 2 years old - 35-30, 2-4 years old - 30-25, 4-6 years old - about 25, 6-12 years old - 22-20, 12-15 years old - 20-18.

Heart massage - a method of resuming and artificially maintaining blood circulation in the body through rhythmic compression of the heart, promoting the movement of blood from its cavities into the great vessels. Used 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 functions of the body. Cardiac massage is not indicated in the absence of blood circulation in the body for a long period of time (biological death) and in the development of irreversible changes in organs that cannot be subsequently replaced by transplantation. Cardiac massage is inappropriate if the patient has injuries to organs that are clearly incompatible with life (primarily the brain); for precisely and predetermined terminal stages of cancer 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 monitor 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 cardioscope screen of his asystole.

A distinction is made between direct (open, transthoracic) cardiac massage, performed with one or two hands through an incision in the chest, and indirect (closed, external) cardiac massage, carried out by rhythmic compression of the chest and compression of the heart between the sternum and spine displaced in the anteroposterior direction.

Mechanism of actiondirect cardiac massage lies in the fact that when the heart is compressed, the blood located in its cavities flows from the right ventricle into the pulmonary trunk and, with simultaneous artificial ventilation of the lungs, 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 therefore to the brain and heart. Restoring the energy resources of the myocardium as a result makes it possible to resume the contractility of the heart and its independent activity during circulatory arrest as a result of ventricular asystole, 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 massage devices.

Direct cardiac massage is often more effective than indirect one, because allows you to directly monitor the state of the heart, feel the tone of the myocardium and promptly eliminate its atony by intracardially injecting solutions of adrenaline or calcium chloride, without damaging the branches of the coronary arteries, since it is possible to visually select an avascular area 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), preference should be given to indirect massage, because To perform a thoracotomy, even in an operating room, certain conditions and time are required, and the time factor in intensive care is decisive. Indirect cardiac massage can be started almost immediately after circulatory arrest is determined and can be performed by any previously trained person.

Monitoring the efficiency of blood circulation , created by cardiac 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 appearance of independent breaths.

The effectiveness of chest compressions is ensured by the correct choice of the place where force is applied to the victim’s chest (the lower half of the sternum immediately above the xiphoid process).

The massager’s hands must 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 put pressure on the victim’s chest) (see. diagrams on the left). They should be straight at the elbow joints. The person performing the massage should stand quite high (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 with the force of his hands, but also with the weight of his body. The pressing force should be sufficient to move 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 per minute. When performing resuscitation by two persons, the massager compresses the chest 5 times with a frequency of approximately 1 time per 1 s, after which the second person providing assistance makes one vigorous and quick exhalation from the mouth to the mouth or nose of the victim. 12 such cycles are carried out in 1 minute. If resuscitation is carried out by one person, then the specified mode of resuscitation measures becomes impossible; the resuscitator is forced to perform indirect cardiac massage at a more frequent rhythm - approximately 15 heart compressions in 12 s, then 2 vigorous blows of air into the lungs in 3 s; 4 such cycles are performed in 1 minute, resulting in 60 heart compressions and 8 breaths. Indirect cardiac massage can only be effective if properly combined with artificial ventilation.

Monitoring the effectiveness of indirect cardiac massage carried out continuously as it progresses. To do this, lift the patient’s upper eyelid with a finger and monitor the width of the pupil. If, within 60-90 seconds of performing a cardiac massage, pulsation in the carotid arteries is not felt, the pupil does not narrow and respiratory movements (even minimal) do not appear, it is necessary to analyze whether the rules for performing a cardiac massage are strictly followed, resort to medication to eliminate myocardial atony, or switch (if conditions exist) to direct cardiac massage.

If signs of the effectiveness of chest compressions appear, 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. Based on the pattern 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.

Failure to comply with the rules for performing chest compressions can lead to complications such as rib fractures, development of pneumo- and hemothorax, liver rupture, etc.

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

3. Post-resuscitation illness. Organization of observation and care for patients. Biological death. Ascertainment of death.

If the resuscitation measures are effective, spontaneous breathing and heart contractions are restored to the patient. He is entering 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 from the start of resuscitation and is characterized by the appearance of consciousness, stabilization of breathing, blood circulation, and metabolism. Regardless of the further prognosis, the patient's condition improves.

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

3. Stage of normalization of functions.

Biological death. Ascertainment of death.

Biological death (or true death) is the irreversible cessation of physiological processes in cells and tissues. Irreversible cessation usually means “irreversible within the framework of modern medical technologies” cessation of processes. Over time, medicine’s ability to resuscitate dead patients changes, as a result of which the borderline of death is pushed into the future. From the point of view of scientists who support cryonics and nanomedicine, most people who are dying now can be revived in the future if the structure of their brain is preserved now.

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

The biological death of a subject does not mean the immediate biological death of the tissues and organs that make up his body. The time before death of the tissues that make up the human body is mainly determined by their ability to survive under conditions of hypoxia and anoxia. This ability is different for different tissues and organs. The shortest life time under anoxic conditions is observed in brain tissue, more precisely, in the cerebral cortex and subcortical structures. The stem sections and spinal cord have greater resistance, or rather resistance to anoxia. Other tissues of the human body have this property to a more pronounced extent. 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. Associated with the phenomenon of survivability of organs and tissues of the human body is the possibility of transplanting them, and the earlier the organs are removed for transplantation after the onset of biological death, 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 gurney specially designed for this purpose on the back with the 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 spots appear).

3. Only after this, the nurse writes down his last name, initials, medical history number on the deceased’s thigh and the corpse is taken to the morgue.

4. Things and valuables are transferred to the relatives or loved ones of the deceased against receipt, according to an inventory drawn up at the time of the patient’s death and certified by at least 3 signatures (nurse, nurse, doctor on duty).

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

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

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

DISEASE - a disorder of the body's vital functions, expressed by physiological and structural changes; occurs under the influence of extraordinary (for a given organism) irritants of the external and internal environment. Environmental factors always play a leading role in the occurrence of a disease, since they not only act directly on the body, but can also cause changes in its internal properties; these changes, being passed on to offspring, may themselves later become the cause of the disease (congenital characteristics). In the body during illness, destructive processes are combined - the result of damage to certain physiological systems (nervous, circulatory, respiration, digestion, etc.) by a pathogenic factor, and restorative processes - the result of the body's counteraction to this damage (for example, increased blood flow, inflammatory reaction, fever and other). Disease processes are characterized by certain signs (symptoms) that distinguish different diseases from each other.

The body's reactions that occur in response to the influence of a pathogenic factor develop differently depending on the properties of the diseased organism. This explains the diversity of the clinical picture and course of the same disease in different individuals. At the same time, each disease has some typical symptoms and course. The branch of pathology (the study of diseases) that studies the mechanisms of disease development is called pathogenesis.

The study of the causes of disease constitutes a branch of pathology called etiology. The causes of the disease may be

1. external factors: mechanical - bruises, wounds, tissue crushing and others; physical - the effect of electric current, radiant energy, heat or cold, changes in atmospheric pressure; chemical - the effect of toxic substances (arsenic, lead, chemical warfare agents and others); biological - living pathogens (pathogenic bacteria, viruses, protozoa, single-celled organisms, worms, ticks, helminths); nutritional disorders - starvation, lack of vitamins in the diet, etc.; mental impact (for example, fear, joy, which can cause dysfunction of the nervous system, cardiovascular, gastrointestinal tract and others; careless words of a doctor can cause serious disorders in suspicious people);
2. internal properties of the body - hereditary, congenital (that is, arising as a result of intrauterine development) and acquired during the subsequent life of a person.

Social factors are extremely important in the occurrence and spread of human disease: difficult working and living conditions of the working masses in a number of capitalist and colonial countries, chronic unemployment, overwork and exhaustion are factors that reduce the body’s resistance and contribute to the spread of the disease and the occurrence of early disability; lack of labor protection leads to the development of severe diseases; wars, which cause injuries and deaths of millions of people, are also the cause of an increase in morbidity among the population. In socialist countries, conditions have been created that promote maximum preservation of workers' health; special health measures at work have led to the elimination of a number of occupational diseases. The socialist health care system favors the prevention of the occurrence and rapid cure of diseases. These circumstances had a dramatic impact on the reduction of morbidity in the USSR and the increase in life expectancy of workers.

During each disease, three periods are distinguished: latent, or hidden; period of precursors, or prodromal; period of severe illness.

• The first, latent period - the time from the onset of action of the pathogenic agent to the appearance of the first symptoms of the disease in infectious diseases; this period is called the incubation period); Its duration varies for different diseases - from several minutes (for example, a burn) to several years (for example, ).
• The second, prodromal period is the time when the first, often unclear, general symptoms of the disease are detected - general malaise, headache, slight rise in temperature.
• The third period, which comes after the prodromal period, is the main one in the course of the disease and is characterized by pronounced symptoms typical of the disease; Its duration varies for different diseases - from several days to tens of years (for example, tuberculosis, syphilis, leprosy). A number of diseases have a definite course (for example, typhoid fever, relapsing fever, pneumonia and others), other diseases do not have such a definite course. Based on the course of the disease and its most characteristic manifestations, the doctor usually makes a diagnosis.

Often, during the course of the disease, complications arise - the appearance of new additional dysfunctions of individual organs or systems (for example, pneumonia in measles, inflammation of the testicle in mumps, bedsores in long-term chronic diseases, in these cases you need to know how to use an anti-bedsore mattress. Sometimes during the course of the disease they arise relapses - the return of the disease after a period of apparent recovery (for example, with typhoid fever, erysipelas, and others).

The outcome of the disease can be: recovery, that is, complete restoration of impaired functions; incomplete recovery, disability - residual effects in the form of persistent weakening of the functions of one or another system - nervous, cardiovascular and others (for example, heart disease after articular rheumatism, immobility of a joint after a tuberculous process in it); transition to a chronic, protracted condition; death. The transition to recovery can occur quickly: a sharp drop in temperature, subsidence of symptoms of the disease - the so-called crisis. Sometimes the transition from illness to recovery occurs slowly, the symptoms of the disease disappear gradually, the temperature does not drop to normal immediately - this is the so-called lysis. Death is usually preceded by agony, lasting from several hours to several days.

Diseases are classified either depending on the damage to certain body systems (disease of the nervous system, respiratory disease, cardiovascular disease, and others) or according to causative factors (infectious diseases, traumatic diseases, nutritional disorders, and so on). In addition, diseases are classified according to the nature of their course: acute, chronic, subacute. Based on the nature of the symptoms and the course of the disease, mild and severe forms of the disease are distinguished.

Treatment of a disease consists of influencing therapeutic factors either on the causes of the disease or on the mechanisms of their development, as well as by mobilizing a number of protective and compensatory adaptations of the body.

A correct understanding of disease, primarily as a result of the interaction of the body with the external environment, determines the preventive direction of socialist health care, which aims primarily to eliminate conditions that can cause disease.