General dysfunctions in surgical diseases. Secondary specialized education of a medical profile. Types of critical conditions

Topic 11. Wounds and wound process. Wound definition and wound symptoms. Types of wounds The concept of single, multiple, combined and combined wounds. Phases 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 using skin grafting.

Purulent wounds, primary and secondary. General and local signs of wound suppuration. Treatment of a purulent wound depending on the phase of the wound process. Application of proteolytic enzymes. Additional methods for treating purulent wounds.

Topic 12. General dysfunctions in a surgical patient. Clinical assessment of the general condition of patients. Types of general disorders of the body's vital functions 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 conditions: preagonia, agony, clinical death. Signs of biological death. First aid for cessation of breathing and circulation. Criteria for the effectiveness of revival. Monitor control systems. Indications for stopping cardiopulmonary resuscitation.

Shock – causes, pathogenesis, clinical picture, diagnosis, phases and stages of surgical shock. First aid for shock. Complex therapy of shock. Criteria for the success of shock treatment. Prevention of surgical shock. The concept of shocks of other etiologies: hemorrhagic shock, cardiogenic shock, anaphylactic shock, septic shock. Intensive therapy of the consequences of acute and chronic blood loss. The concept of hypoventilation. Diagnosis of insufficiency of external respiration function. Equipment for artificial lung ventilation (ALV). Indications for the use and administration of mechanical ventilation. Tracheostomy, tracheostomy care. Diagnosis and intensive treatment of disorders of the motor-evacuation function of the digestive tract. Diagnosis of the main syndromes of water-electrolyte and acid-base balance disorders. Principles of drawing up a corrective program. Intensive therapy for 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 injuries. Complications and dangers of injuries: immediate, immediate and late. General principles of diagnosing traumatic injuries, providing first aid and treatment. Nonspecific and specific prevention of infectious complications.

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

Types of mechanical damage to tendons, bones and joints. Ligament and tendon ruptures. Traumatic dislocations. Joint bruises, Hemarthrosis, First aid and treatment. Bone fractures. Classification. Clinical symptoms of fractures. Basics of X-ray diagnostics of dislocations and fractures. The concept of fracture healing. The process of callus 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 damage to the spinal cord. 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 treatment of fractures: reposition, immobilization, surgical treatment. The concept of plaster casts. Plaster. Basic rules for applying plaster casts. 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 lives of patients. Objectives of first aid for head injury. Measures for their implementation. Features of transporting 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, one- and two-sided. The concept of pneumothorax. Types of pneumothorax: open, closed, valve (tension) external and internal. First aid and transportation features for tension pneumothorax, hemoptysis, foreign bodies in the lungs, open and closed injuries to the lungs, heart and great vessels. Features of gunshot wounds to the chest, first aid, transportation of the victim.

Injuries to the abdomen with or 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 abdominal injuries: acute anemia, peritonitis.

Features of treatment 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. Classification of burns. Recognizing the depth of burns. Determination of burn area. Prognostic methods for determining the severity of a burn.

First aid for burns. Primary surgical treatment of the burn surface: anesthesia, asepsis, surgical technique. Treatment methods for local treatment of burns: open, closed, mixed. Skin grafting. Antimicrobial therapy (sulfonamides, antibiotics, serums). Outpatient treatment of burns: indications, contraindications, methods. Reconstructive and plastic surgery of post-burn scar 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).

Injuries from cooling. Types of cold injury: general – freezing and chills; local – frostbite. Prevention of cold injury in peacetime and war. Symptoms of freezing and chills, first aid for them and further treatment.

Classification of frostbite by degree. 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 during 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 trauma. The effect of electric current on the human body. The concept of electropathology. Local and general action 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. Impact of caustic chemicals on tissue. Features of local manifestation. First aid for chemical burns of the skin, mouth, esophagus, stomach. Complications and consequences of esophageal burns.

Features of treatment tactics in outpatient settings.

Topic 15. Fundamentals of purulent-septic surgery. General issues of surgical infection. The concept of surgical infection. Classification of surgical infections: 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 surgical techniques. Modern methods of treating purulent lesions and methods of postoperative management. General treatment for purulent diseases: rational antibacterial therapy, immunotherapy, complex infusion therapy, hormone and enzyme therapy, symptomatic therapy.

Acute aerobic surgical infection . Main pathogens. Routes of infection. 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 exhaustion.

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.

The 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, periwound pyoderma. Clinic, features of the course and treatment. Types of purulent-inflammatory diseases of the subcutaneous tissue: abscess, cellulite, phlegmon. Clinic, diagnostics, local and general treatment. Possible complications. Purulent diseases of the lymphatic and blood vessels.

Purulent hand surgery. The concept of felon. Types of felon. Boils 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 . Cellulitis of the neck. Axillary and subpectoral phlegmon. Subfascial and intermuscular phlegmon of the extremities. Phlegmons of the foot. Purulent mediastinitis. Purulent processes in the tissue of the retroperitoneum and pelvis. Purulent paranephritis. Purulent and chronic acute paraproctitis. Causes of occurrence, 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 lactation postpartum mastitis.

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

Purulent surgery of serous cavities. An idea of ​​the etiology, clinical manifestations and principles of treatment of purulent meningitis and brain abscesses. Acute purulent pleurisy and pleural empyema. Pericarditis. Purulent lung diseases: abscess and gangrene of the lung, chronic suppurative lung diseases. General understanding of the causes, symptoms, diagnosis and treatment (conservative and surgical).

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.

Features of diagnostics and treatment tactics in outpatient settings.

Topic 17. Purulent surgery of bones and joints. General purulent surgical infection. Purulent bursitis. Purulent arthritis. Causes, clinical picture, principles of treatment. Osteomyelitis. Classification. The concept of exogenous (traumatic) and endogenous (hematogenous) osteomyelitis. Modern "idea of ​​the etiopathogenesis of hematogenous osteomyelitis. Symptoms of acute osteomyelitis. The concept of primary-chronic forms of osteomyelitis. Chronic recurrent osteomyelitis. Diagnosis of various forms of osteomyelitis. Principles of general and local (operative and non-operative) treatment of osteomyelitis.

Concept of sepsis. Types of sepsis. Etiopathogenesis. An idea of ​​the entrance gate, the role of macro- and microorganisms in the development of sepsis. Clinical forms of the course and clinical picture of sepsis. Diagnosis of sepsis. Treatment of sepsis: surgical sanitation of a purulent focus, general replacement and corrective therapy.

Features of diagnostics and treatment tactics in outpatient settings.

Topic 18. Acute and chronic specific infection. The concept of a specific infection. Main diseases: tetanus, anthrax, rabies, wound diphtheria. Tetanus is an acute specific anaerobic infection. Ways and conditions of penetration and development of tetanus infection.

Incubation period. Clinical manifestations. Prevention of tetanus: specific and nonspecific. The importance of early diagnosis of tetanus. Complex symptomatic treatment of tetanus. Anthrax and diphtheria of wounds: features of the clinical picture, treatment, isolation of the patient.

The concept of chronic specific infection. Surgical tuberculosis in children and adults. Forms of surgical tuberculosis. The most common forms of osteoarticular tuberculosis. Features of tuberculous sintered (cold) abscess Diagnosis and complex treatment of osteoarticular tuberculosis. Local treatment of edema abscesses and fistulas. Surgical forms of pulmonary tuberculosis. Tuberculous lymphadenitis.

Actinomycosis. Clinical picture, differential diagnosis, complex therapy.

The concept of surgical syphilis.

Features of diagnostics and treatment tactics in outpatient settings.

Topic 19. Fundamentals of surgery for circulatory disorders and necrosis. Necrosis. Circulatory disorders that can cause necrosis. Other factors leading to local (limited or widespread) tissue necrosis. Types of necrosis, local and general manifestations. Gangrene is dry and wet.

Arterial blood flow disorders: acute and chronic. General principles of clinical and instrumental diagnostics. Surgical and conservative treatment. First aid for acute thrombosis and arterial embolism.

Venous circulation disorders: acute and chronic. The concept of phlebothrombosis, phlebitis, thrombophlebitis. The concept of pulmonary embolism. Other peripheral venous diseases and their complications. Trophic ulcers, principles of surgical and non-operative treatment. First aid for acute thrombosis and thrombophlebitis, bleeding from varicose ulcers, pulmonary embolism.

Bedsores as a particular type of necrosis. Causes of occurrence. Dynamics of bedsore development. Prevention of bedsores: features of care for patients who stay in bed for a long time. Local treatment of bedsores. The significance and nature of general measures in the treatment of pressure ulcers.

Features of diagnostics and treatment tactics in outpatient settings.

Topic 20. Fundamentals of tumor surgery. The concept of benign and malignant tumors. Precancerous diseases. Features of the clinical picture and development of the disease in benign and malignant neoplasms. Clinical classification of tumors. Surgical treatment of benign tumors. Preventive examinations. Organization of oncology service. Principles of complex therapy of malignant tumors and the place of surgical methods in the treatment of tumors.

Features of diagnostics and treatment tactics in outpatient settings.

Types of depression of consciousness Fainting - generalized muscle weakness, inability to stand upright, loss of consciousness. Coma is a complete shutdown of consciousness with a total loss of perception of the environment and oneself. Collapse is a drop in vascular tone with a relative decrease in circulating blood volume.

Degrees of impairment of consciousness Stupor – unconsciousness, preservation of defensive movements in response to painful and sound stimuli. Moderate coma – inability to wake up, lack of defensive movements. Deep coma - suppression of tendon reflexes, loss of muscle tone. Terminal coma is an agonal state.

Assessment of the depth of impairment of consciousness (Glasgow scale) Clear consciousness 15 Stunning Stupor 9-12 Coma 4-8 Brain death 3

Emergency care for loss of consciousness Eliminate etiological factors. Place the patient in a horizontal position with the leg end raised. Ensure free breathing: unfasten the collar and belt. Give stimulants (ammonia, vinegar) to inhale. Rub the body, cover with warm heating pads. Inject 1% mezaton 1 ml IM or s/c 10% caffeine 1 ml. For severe hypotension and bradycardia, 0.1% atropine 0.5-1 ml.

Physiology of respiration The breathing process The breathing process is conventionally divided into 3 stages: The first stage includes the delivery of oxygen from the external environment to the alveoli. The second stage involves the diffusion of oxygen through the alveolar membrane of the acinus and its delivery to the tissues. The third stage includes the utilization of oxygen during the biological oxidation of substrates and the formation of energy in cells. If pathological changes occur at any of these stages, ARF may occur. With ARF of any etiology, there is a disruption in the transport of oxygen to tissues and the removal of carbon dioxide from the body.

Indicators of blood gases in a healthy person Indicator Arterial blood Mixed blood p O 2 mm Hg. st SaO 2, % pCO 2, mm Hg. st

Etiological classification of ARF PRIMARY (stage 1 pathology - oxygen delivery to the alveoli) Causes: mechanical asphyxia, spasm, tumor, vomit, pneumonia, pneumothorax. SECONDARY (stage 2 pathology - oxygen transport from the alveoli to the tissues is impaired) Causes: microcirculation disorders, hypovolemia, pulmonary embolism, cardiogenic pulmonary edema.

The main syndromes of ARF 1. Hypoxia is a condition that develops with a decrease in tissue oxygenation. Exogenous hypoxia - due to a decrease in the partial pressure of oxygen in the inhaled air (submarine accidents, high altitudes). Hypoxia due to pathological processes that disrupt the supply of oxygen to tissues at its partial pressure.

Hypoxia due to pathological processes is divided into: a) respiratory (alveolar hypoventilation - obstruction of the airways, reduction of the respiratory surface of the lungs, respiratory depression of central origin); b) circulatory (against the background of acute and chronic circulatory failure); c) tissue (potassium cyanide poisoning - the process of oxygen absorption by tissues is disrupted); d) hemic (decrease in red blood cell mass or hemoglobin in red blood cells).

3. Hypoxemic syndrome is a violation of oxygenation of arterial blood in the lungs. An integral indicator is a reduced level of partial oxygen tension in arterial blood, which occurs in a number of parenchymal lung diseases. Main syndromes of ARF

Clinical stages of ARF Stage I: Consciousness: preserved, anxiety, euphoria. Respiratory function: lack of air, respiratory rate per minute, mild acrocyanosis. Blood circulation: heart rate per minute. BP is normal or slightly elevated. The skin is pale and moist. Partial pressure of O 2 and CO 2 of blood: p O 2 up to 70 mm Hg. p CO 2 up to 35 mmHg.

Stage II: Consciousness: impaired, agitation, delirium. Respiratory function: severe suffocation, respiratory rate per minute. Cyanosis, sweating of the skin. Blood circulation: heart rate per minute. Blood pressure Partial pressure of O 2 and CO 2 of blood: p O 2 to 60 mm Hg. p CO 2 up to 50 mmHg. Clinical stages of ARF

Stage III: Consciousness: absent, clonic-tonic convulsions, pupils dilated, do not respond to light. Respiratory function: tachypnea 40 or more per minute turns into bradypnea 8-10 per minute, spotty cyanosis. Blood circulation: heart rate more than 140 per minute. Blood pressure, atrial fibrillation. Partial pressure of O 2 and CO 2: p O 2 up to 50 mmHg. p CO 2 to mmHg. Clinical stages of ARF

Emergency care for acute respiratory failure 1. Restoration of airway patency. 2. Elimination of alveolar ventilation disorders (local and general). 3. Elimination of central hemodynamic disorders. 4. Correction of the etiological factor of ARF. 5. Oxygen therapy 3-5 l/min. at stage I ARF. 6. At stages II – III of ARF, tracheal intubation and artificial ventilation are performed.

Treatment of AHF 1. Subcutaneous administration of 1-2 ml of morphine, preferably combined with the administration of 0.5 ml of a 0.1% solution of atropine sulfate; 2. Nitroglycerin under the tongue - 1 tablet or 1-2 drops of 1% solution on a piece of sugar; 3. Analgesics: baralgin 5.0 IV, IM, no-shpa 2.0 IM, analgin 2.0 IM. 4. For cardiac arrhythmias: lidocaine mg IV, procainamide 10% 10.0 IV, obzidan 5 mg IV. 5. For pulmonary edema: dopmin 40 mg IV on glucose, Lasix 40 mg IV, aminophylline 2.4% 10.0 IV.

ETIOLOGY OF AKI 1. Traumatic, hemorrhagic, blood transfusion, bacterial, anaphylactic, cardiogenic, burn, surgical shock; electrical trauma, postpartum sepsis, etc. 2. Acute infarction of the kidney. 3. Vascular abstraction. 4. Urological abstraction.

DIAGNOSTICS 1. Decreased diuresis (less than 25 ml/h) with the appearance of protein, red blood cells, leukocytes, casts, decreased urine density to 1.005-1, increased azotemia (16.7-20.0 mmol/l). 3. Hyperkalemia. 4. Decrease in blood pressure. 5. Decrease in hemoglobin and red blood cells.

Prevention and treatment of acute renal failure 1. Sufficient pain relief for injuries. 2. Elimination of hypovolemia. 3. Elimination of water and electrolyte disturbances. 4. Correction of cardiodynamics and rheology. 5. Correction of respiratory function. 6. Correction of metabolic disorders. 7. Improving blood supply to the kidneys and eliminating foci of infection in them. 8. Antibacterial therapy. 9. Improving rheology and microcirculation in the kidneys. 10. Extracorporeal detoxification (hemodialysis). 11. Osmodiuretics (Manitol 20% 200.0 IV), saluretics (Lasix mg IV).

Classification of acute liver disease 1. Endogenous – it is based on massive necrosis of the liver, resulting from direct damage to its parenchyma; 2. Exogenous (portocaval) – the form develops in patients with liver cirrhosis. In this case, the metabolism of ammonia by the liver is disrupted; 3. Mixed form.

CLINICAL MANIFESTATIONS OF OPEN 1. Depression of consciousness up to coma 2. Specific “liver odor” from the mouth 3. Icterus of the sclera and skin 4. Signs of hemorrhagic syndrome 5. Appearance of areas of erythema in the form of stellate angiomas 6. Jaundice 7. Ascites 8. Splenomegaly

LABORATORY DIAGNOSTICS Study of liver functions (increased bilirubin, transaminases, decreased protein), kidneys (azotemia), acid-base balance (metabolic acidosis), water and electrolyte metabolism (hypokalemia, hyponatremia), blood coagulation system (hypocoagulation).

Principles of treatment for APE 1. Eliminate bleeding and hypovolemia. 2. Eliminate hypoxia. 3. Detoxification. 4. Normalization of energy metabolism. 5. Use of hepatotropic vitamins (B 1 and B 6), hepatoprotectors (essentiale). 6. Normalization of protein metabolism. 7. Normalization of water-electrolyte metabolism, acid-base balance. 8. Normalization of the blood coagulation system.

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, performed 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.

Main clinical characteristics of assessing the state of consciousness:

Clear consciousness – its complete preservation, adequate reaction to the environment, full orientation, wakefulness.

Moderate stupor - moderate drowsiness, partial disorientation, delay in answering questions (repetition is often required), slow execution of commands.

Deep stupor - deep drowsiness, disorientation, limitation and difficulty in speech contact, and only performing simple commands.

Stupor (unconsciousness, sound sleep) - almost complete absence of consciousness, preservation of targeted, coordinated defensive movements, opening of eyes to painful and sound stimuli, occasional monosyllabic answers to questions, loss of control over pelvic functions.

Moderate coma (I) - lack of consciousness, chaotic uncoordinated movements in response to painful stimuli, failure to open the eyes in response to stimuli.

Deep coma (II) – lack of consciousness and protective movements, impaired muscle tone, inhibition of tendon reflexes, respiratory and cardiovascular disorders.

Transcendental (terminal) coma (III) – agonal state, atony, areflexia, vital functions are supported by mechanical ventilation and cardiovascular drugs.

The clinic distinguishes 5 degrees of severity of the patient’s general condition:

A satisfactory state is a clear consciousness. Vital functions (VF) are not impaired.

The state is of moderate severity – consciousness is clear or there is moderate stun. The vital functions are slightly damaged.

Severe condition - consciousness is impaired to the point of deep stupor or stupor. Severe disturbances in the functioning of the respiratory and/or cardiovascular systems.

The condition is extremely serious - moderate or deep coma, severe symptoms of damage to the respiratory and/or cardiovascular systems.

The terminal state is an extreme coma with gross signs of damage to the trunk and disturbances of vital functions.

Types of dysfunction of the body. Acute respiratory failure.

Acute respiratory failure (ARF)) is a syndrome based on disturbances in the external respiratory 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 tension of this system.

Etiology.

There are pulmonary and extrapulmonary causes of the development of ARF.

Extrapulmonary causes:

Violation of central regulation of breathing: a) acute vascular disorders (acute cerebrovascular accidents, 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; d) comatose states.

Damage to the musculoskeletal system 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) polio, tetanus; e) spinal cord injuries; f) consequences of the action of organophosphorus compounds and muscle relaxants.

ARF due to impaired oxygen transport due to large blood losses, acute circulatory failure and poisoning (carbon monoxide).

Pulmonary causes:

Obstructive disorders: a) blockage of the airways with a foreign body, sputum, vomit; b) mechanical obstruction to air access due to external compression (hanging, suffocation); c) allergic laryngo- and bronchospasm; d) tumor processes of the respiratory tract; e) violation of the act of swallowing, paralysis of the tongue with its retraction; f) edematous-inflammatory diseases of the bronchial tree.

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

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

Classification of ODN.

Etiological:

Primary ARF is associated with impaired oxygen delivery to the alveoli.

Secondary ARF is associated with impaired oxygen transport from the alveoli to the tissues.

Mixed ARF is a combination of arterial hypoxemia with hypercapnia.

Pathogenetic:

The ventilation form of ARF occurs when the respiratory center is damaged of any etiology, when there is a disturbance in the transmission of impulses in the neuromuscular system, damage to the chest and lungs, or a change in the normal mechanics of breathing due to pathology of the abdominal organs (for example, intestinal paresis).

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

Pathogenesis of ARF is caused by the development of oxygen starvation of the body as a result of disturbances in alveolar ventilation, diffusion of gases through alveolar-capillary membranes and uniform distribution of oxygen throughout organs and systems.

Highlight three main syndromes ONE:

I .Hypoxia– a condition that develops as a consequence of reduced tissue oxygenation.

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

A). Hypoxia due to reduced partial pressure of oxygen in the inspired 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 tension in the inhaled air:

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

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

Tissue hypoxia – disruption of oxygen absorption processes at the tissue level (potassium cyanide poisoning)

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

II. Hypoxemia– disruption 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), when blood flow in the lungs predominates over ventilation during airway obstruction, or when the diffusion capacity of the alveolar-capillary membrane is impaired during respiratory distress syndrome. An integral indicator of hypoxemia is the level of partial oxygen tension in arterial blood (P a O 2 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, in 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, bronchial secretion and blood pressure (BP) increase. 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 (P and CO 2 is normally 35-45 mm Hg).

Clinical picture.

Shortness of breath, disturbance of the breathing rhythm: tachypnoe, accompanied by a feeling of lack of air with the participation of auxiliary muscles in the act of breathing, with increasing hypoxia - bradypnea, Cheyne-Stokes, Biot breathing, with the development of acidosis - Kussmaul breathing.

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

The clinic isolates three stages of ARF.

Istage I. The patient is conscious, restless, and may be euphoric. Complaints of feeling short of air. The skin is pale, moist, mild acrocyanosis. Respiration number (RR) - 25-30 per minute, heart rate (HR) - 100-110 beats/min, blood pressure within normal limits or slightly increased, P a O 2 70 mm Hg, P a CO 2 35 mmHg. (hypocapnia is compensatory in nature, as a result of shortness of breath).

IIstage. Complaints of severe suffocation. Psychomotor agitation. Delirium, hallucinations, and loss of consciousness are possible. The skin is cyanotic, sometimes in combination with hyperemia, profuse sweat. RR - 30 - 40 per minute, heart rate - 120-140 beats/min, arterial hypertension. Pa O 2 decreases to 60 mm Hg, Pa CO 2 increases to 50 mm Hg.

IIIstage. There is no consciousness. Cramps. Dilated pupils with lack of reaction to light, spotty cyanosis. Bradypnea (RR – 8-10 per minute). Blood pressure drop. Heart rate more than 140 beats/min, arrhythmias. Pa O 2 decreases to 50 mm Hg, Pa CO 2 increases to 80 - 90 mm Hg. and more.

General dysfunctions in acute surgical diseases of the abdominal organs are mainly caused by intoxication.

Endogenous intoxication- (Latin in in, inside + Greek toxikon poison) - a disruption of life caused by toxic substances formed in the body itself.

Endotoxicosis(endotoxicoses; Greek endō inside + toxikon poison + -ōsis) - complications of various diseases associated with disruption of homeostasis due to the accumulation in the body of endogenous toxic substances with pronounced biological activity. In clinical practice, endotoxemia is usually considered as a syndrome of endogenous intoxication that occurs with acute or chronic failure of the body's natural detoxification system (inability to effectively remove metabolic products). In contrast to intoxication, endotoxemia refers to an already formed state of poisoning with substances of an endogenous nature, and the term “intoxication” refers to the entire pathological process of intense self-poisoning of the body.

To refer to the processes of eliminating endotoxemia, the terms “detoxification” and “detoxification” are used. The latter term is more often used to describe therapeutic methods of enhancing the natural processes of cleansing the body.

Clinical signs of endotoxicosis have been known for a long time. In almost any disease, especially of an infectious nature, children and adults develop symptoms characteristic of “endogenous intoxication”: weakness, stupor, nausea and vomiting, loss of appetite and weight loss, sweating, pale skin, tachycardia, hypotension, etc. These most typical signs are usually divided into groups. The phenomena of neuropathy (encephalopathy), which are based on dysfunctions of the nervous system (neurotoxicosis), are often the first prodromal symptoms of developing intoxication, since the most highly differentiated nerve cells of the brain are especially sensitive to metabolic disorders and hypoxia. In children, dysfunctions of the nervous system are most severe with the development of psychomotor agitation, convulsions, soporous or even comatose states. In infectious diseases, a feverish state with signs of intoxication psychosis is typical. Manifestations of cardiovasopathy can be in the nature of mild asthenovegetative disorders and severe circulatory disorders of a hypodynamic type (decrease in stroke volume of the heart, increase in total peripheral vascular resistance, cardiac rhythm and conduction disturbances), usually accompanied by respiratory failure (shortness of breath, cyanosis of the mucous membranes, metabolic acidosis). Hepato- and nephropathy are most often manifested by proteinuria, oliguria, azotemia, and sometimes liver enlargement and jaundice are noted.

Laboratory diagnostics. To assess the severity of toxemia and monitor the dynamics of its development, quite a few laboratory tests have been proposed. One of the first to use integral indicators of blood plasma (lymph) toxicity was the leukocyte intoxication index and the neutrophil shift index.

For laboratory assessment of the severity of homeostasis disorders accompanying endotoxemia, traditional methods are used that characterize the main functions of the affected organ (for example, in case of nephropathy, the composition of urine, the concentration of creatinine, urea in plasma, etc. are examined; in case of hepatopathy, a blood test is performed for bilirubin, transaminases, proteins, cholesterol etc.) or a certain body system that usually suffers from endotoxicosis. This is primarily the acid-base state, osmolarity, rheological data (relative viscosity, aggregation of erythrocytes and platelets) and basic immunological indicators (level of T- and B-lymphocytes, immunoglobulins of class G, A, M, etc.).

Some laboratory biochemical tests are specific for this type of lesions that cause endotoxemia, for example, determination of myoglobin in the blood and urine in case of injury, enzyme activity in case of pancreatitis, bacteremia in case of sepsis.

1) etiological, which aims to accelerate the removal of toxic substances from the body using methods of enhancing natural detoxification and methods of “artificial detoxification”;

2) pathogenetic, associated with the need to reduce the intensity of catabolic processes and the activity of proteolytic enzymes, increase the immunological defense of the body;

3) symptomatic, with the task of maintaining the function of the cardiovascular and respiratory systems.

In addition, the entire arsenal of treatments for the underlying disease, which led to the development of endotoxemia, is simultaneously used. Most often this is antibacterial treatment, specific pharmacotherapy, surgical treatment, etc.

For the purpose of detoxification, intravenous infusion therapy (solutions of glucose, electrolytes, hemodez) is most widely used, often in combination with the method of forced diuresis using osmotic diuretics (urea, mannitol in a dose of 1-1.5 g/kg) in the form of hypertonic solutions (15-20%) or saluretics (furosemide in a dose of up to 500-800 mg per day).

To remove toxins from the blood, hemofiltration is used ( hemodialysis )or hemosorption, as well as plasmapheresis surgery (purification of blood plasma). In cases of overhydration of the body or high concentrations of toxins in the blood and lymph, it is recommended lymphatic drainage and cleansing the resulting lymph (lymphosorption) with its subsequent return to the body (intravenous drip infusions) to avoid possible loss of proteins.

The greatest effectiveness of detoxification is achieved with the combined use of several methods and the use of various biological media (blood, lymph) for cleansing.

Pathogenetic treatment of endotoxemia consists of the use of antiproteolytic drugs (contrical, trasylol or ingitril), antioxidants (tocopherol), immunostimulants (T-activin).

Ultraviolet irradiation of blood in a dose of up to 100-120 has the greatest effect in this regard. J, carried out daily in the amount of 5-6 procedures.

Detoxification and pathogenetic treatment should be carried out under the control of the dynamics of the concentration of SM and other laboratory indicators of endotoxemia until they are stable and normalized.

Forecast is largely related to the possibilities of using modern methods of artificial detoxification in the early stages of the development of endotoxemia.