Syndromes of violation of vital functions of the body. Lecture Topic: "Critical Vital Disorders in Surgical Patients" Clinical assessment of the general condition of patients
General disorders of vital activity in acute surgical diseases of the abdominal organs are mainly due to intoxication.
Endogenous intoxication- (Latin in in, inside + Greek toxikon poison) - a violation of vital activity caused by toxic substances formed in the body itself.
Endotoxicoses(endotoxicoses; Greek endō inside + toxikon poison + -ōsis) - complications of various diseases associated with a violation of homeostasis due to the accumulation in the body of endogenous toxic substances with pronounced biological activity. In clinical practice, endotoxicosis is usually considered as a syndrome of endogenous intoxication that occurs in acute or chronic insufficiency of the function of the body's natural detoxification system (inability to effectively remove metabolic products). In contrast to intoxication, endotoxicosis refers to the already formed state of poisoning with endogenous substances, and the term "intoxication" refers to the entire pathological process of intensive self-poisoning of the body.
The terms "detoxification" and "detoxification" are used to refer to the processes of eliminating endotoxicosis. The latter term is more often used to characterize therapeutic methods of enhancing the body's natural cleansing processes.
Clinical signs of endotoxicosis 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, pallor of the 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, dysfunction of the nervous system is most severe with the development of psychomotor agitation, convulsions of soporous or even coma. In infectious diseases, a febrile 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 the hypodynamic type (decrease in stroke volume of the heart, increase in total peripheral vascular resistance, rhythm and conduction disturbances of the heart), 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, sometimes there is an increase in the liver and jaundice.
Laboratory diagnostics. To assess the severity of toxemia and control the dynamics of its development, quite a lot of laboratory tests have been proposed. One of the first to use integral indicators of the toxicity of blood plasma (lymph) - leukocyte intoxication index and neutrophil shift index.
For laboratory assessment of the severity of homeostasis disorders associated with endotoxicosis, traditional methods are used that characterize the main functions of the affected organ (for example, with nephropathy, the composition of urine, the concentration of creatinine, plasma urea, etc. are examined; with hepatopathy, a blood test is performed for bilirubin, transaminases, proteins, cholesterol etc.) or a certain system of the body, usually suffering from endotoxicosis. This is primarily the acid-base state, osmolarity, rheological data (relative viscosity, aggregation of erythrocytes and platelets) and basic immunological parameters (the level of T- and B-lymphocytes, class G, A, M immunoglobulins, etc.).
Some laboratory biochemical studies are specific for this type of lesions that cause endotoxicosis, for example, the determination of myoglobin in the blood and urine in trauma, enzyme activity in pancreatitis, bacteremia in sepsis.
1) etiological, which aims to accelerate the elimination of toxic substances from the body using methods to enhance 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 endotoxicosis, is simultaneously used. Most often, this is antibacterial treatment, specific pharmacotherapy, surgical aid, etc.
For the purpose of detoxification, intravenous infusion therapy (solutions of glucose, electrolytes, gemodez) is most widely used, often in combination with the method of forced diuresis using osmotic diuretics (urea, mannitol at a dose of 1-1.5 g/kg) in the form of hypertonic solutions (15-20%) or saluretics (furosemide at a dose of up to 500-800 mg per day).
Hemofiltration is used to remove toxins from the blood hemodialysis )or hemosorption, as well as the operation of plasmapheresis (purification of blood plasma). With symptoms of hyperhydration of the body or a high concentration of toxins in the blood and lymph, it is recommended lymphatic drainage and purification of the resulting lymph (lymphosorption) with its subsequent return to the body (intravenous drip infusion) to avoid possible loss of proteins.
The highest efficiency of detoxification is achieved with the combined use of several methods and the use of various biological media (blood, lymph) for purification.
Pathogenetic treatment of endotoxicosis consists in the use of antiproteolytic drugs (kontrykal, trasilol or ingitril), antioxidants (tocopherol), immunostimulants (T-activin).
The greatest effect in this respect has ultraviolet blood irradiation at a dose of up to 100-120 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 endotoxicosis until their stable normalization.
Forecast is largely associated with the possibility of using modern methods of artificial detoxification in the early stages of the development of endotoxicosis.
DISEASE - a violation of the vital activity of the body, expressed by physiological and structural changes; arises 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 onset of a disease, since they not only act directly on the body, but can also cause changes in its internal properties; these changes, being transmitted to offspring, in the future may themselves become the cause of the disease (congenital features). In the body during an 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 resistance to this damage (for example, increased blood flow, inflammatory reaction, fever, etc.). other). Painful processes are characterized by certain signs (symptoms) that distinguish various diseases from each other.
The reactions of the body 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 the course of the same disease in different individuals. At the same time, each disease has some typical symptoms and course. The section of pathology (the doctrine of diseases), which studies the mechanisms of the development of the disease, is called pathogenesis.
The study of the causes of the disease is a branch of pathology called etiology. Causes of illness can be
- external factors: mechanical - bruises, wounds, tissue crushing and others; physical - the action of electric current, radiant energy, heat or cold, changes in atmospheric pressure; chemical - the action of toxic substances (arsenic, lead, chemical warfare agents and others); biological - live pathogens (pathogenic bacteria, viruses, protozoa, unicellular organisms, worms, ticks, helminths); malnutrition - starvation, lack of vitamins in the diet, and others; mental impact (for example, fear, joy, which can cause dysfunctions of the nervous system, cardiovascular, gastrointestinal tract and others; careless words of a doctor can cause serious disorders in suspicious people);
- the internal properties of the body - hereditary, congenital (that is, resulting from intrauterine development) and acquired during the subsequent life of a person.
In the emergence and spread of human disease, social factors are of exceptional importance: the difficult working and living conditions of the working masses of 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 emergence of early disability; the lack of labor protection leads to the development of severe; wars that cause injury and death of millions of people are at the same time the cause of an increase in the incidence of the population. Conditions have been created in the socialist countries that are conducive to the maximum preservation of the health of the working people; special health-improving measures in production led to the elimination of a number of occupational diseases. The socialist health care system is conducive to the prevention of the onset and speedy cure of diseases. These circumstances were sharply reflected in the decrease in morbidity in the USSR and in the increase in the 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 the action of the pathogen to the appearance of the first symptoms of the disease in infectious diseases, this period is called the incubation period); its duration in different diseases is different - from several minutes (for example, a burn) to several years (for example, ).
- The second, prodromal period is the time when the first, often obscure, general symptoms of the disease are detected - general malaise, headache, a slight rise in temperature.
- The third period, following the prodrome, is the main one in the course of the disease and is characterized by pronounced symptoms typical of this disease; its duration varies with different diseases - from several days to tens of years (for example, tuberculosis, syphilis, leprosy). A number of diseases have a definite period of course (for example, typhoid fever, relapsing fever, pneumonia, and others), other diseases do not have such a definite period of course. According to the course of the disease, according to its most characteristic manifestations, the doctor usually makes a diagnosis.
Often complications arise during the course of the disease - the appearance of new additional violations of the functions of individual organs or systems (for example, pneumonia with measles, testicular inflammation with mumps, bedsores with long-term chronic diseases, in these cases you need to know how to use an anti-decubitus mattress. Sometimes during the course of the disease there are relapses - the return of the disease after an interval of apparent recovery (for example, with typhoid fever, erysipelas and others).
The outcomes of the disease can be: recovery, that is, complete restoration of impaired functions; incomplete recovery, disability - residual effects in the form of a persistent weakening of the functions of one or another system - nervous, cardiovascular and others (for example, heart disease after articular rheumatism, joint immobility after a tuberculous process in it); transition to a chronic, protracted state; death. The transition to recovery can occur quickly: a sharp drop in temperature, subsidence of the symptoms of the disease - the so-called crisis. Sometimes the transition from illness to recovery is slow, 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.
The disease is classified either depending on the damage to certain body systems (disease of the nervous system, respiratory disease, disease of the cardiovascular system, and others) or by causal factors (infectious, traumatic diseases, malnutrition, and so on). In addition, diseases are classified according to the nature of the course: acute, chronic, subacute. According to the nature of the symptoms and the course of the disease, mild and severe forms of the disease are distinguished.
The treatment of a disease consists in the influence of 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 organism's interaction with the external environment, determines the preventive direction of socialist health care, which aims primarily to eliminate the conditions that can cause disease.
During the study of the topic, the student must have the following professional competencies:
Able and willing to identify critical life dysfunctions in surgical patients
Able and ready to provide first aid in case of critical disorders of life
I. Motivation for the purpose of the lesson
Knowledge of critical disorders of vital activity is necessary not only for the professional activity of a doctor of any specialty, but also in the daily life of a person, because. allows you to master the 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 in such conditions as acute respiratory failure, acute cardiovascular failure, acute renal and hepatic failure, multiple organ failure syndrome.
III. Educational targets
After self-study of the material of this topic, the student should
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 to diagnose acute respiratory failure, acute heart failure, acute renal and hepatic failure, multiple organ failure syndrome based on clinical symptoms;
Ø to 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 adolescents of a surgical profile.
IV. Initial level of knowledge
The student must repeat the concept of first aid, indicators of the state of the functions of vital organs (BP, pulse, frequency and amplitude of respiratory movements, etc.).
V. Plan for studying the topic
1. Clinical assessment of the general condition.
2. Types of violation of the vital activity of the organism in surgical patients.
3. Causes, mechanisms of development, principles of diagnosis and treatment of acute respiratory failure.
4. Causes, mechanisms of development, principles of diagnosis and treatment of acute heart failure.
5. Causes, mechanisms of development, principles of diagnosis and treatment of acute renal failure.
6. Causes, mechanisms of development, principles of diagnosis and treatment of acute liver failure.
7. Causes, mechanisms of development, principles of diagnosis and treatment of multiple organ failure syndrome.
1. Sumin, S.A. Emergency conditions: textbook. allowance for medical students. universities / S.A. Sumin. 6th ed., revised. and additional - M.: MIA, 2006. - 799 p.: ill. (Study literature for students of medical universities and faculty).
2. Practical skills and abilities in the course "General Surgery": textbook. manual for students of all faculties / ed. B.S. Sukovatykh; GOU VPO "Kursk. state. medical. un-ta", 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 medical faculty of Kursk KSMU 2012.
Electronic Library of the Medical University "Student Advisor" 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.
Acute respiratory failure- a syndrome based on violations of the function of external respiration, leading to an insufficient supply of oxygen or a delay in the body of CO2. 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 and hypercapnia rapidly progress, and blood pH decreases. Violations of oxygen and CO2 transport 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 proper treatment, a fatal outcome is possible.
Clinical forms of acute respiratory failure
Etiology and pathogenesis
Acute respiratory failure occurs when violations in the chain of regulatory mechanisms, including the 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 (lung parenchyma, capillaries and alveoli), accompanied by significant disorders of gas exchange. To this it should be added that the "mechanics of breathing", that is, the work of the lungs as an air pump, can also be disturbed, for example, as a result of trauma or deformation of the chest, pneumonia and hydrothorax, high standing of the diaphragm, weakness of the respiratory muscles and (or) airway obstruction. The lungs are the “target” organ that reacts to any changes in metabolism. Mediators of critical conditions pass through the lung filter, causing damage to the ultrastructure of the lung tissue. Pulmonary dysfunction of one degree or another always occurs with severe effects - trauma, shock or sepsis. Thus, the etiological factors of acute respiratory failure are extremely extensive and diverse.
In the practice of intensive care, two types of acute respiratory failure are distinguished: 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 the content of CO2 in the blood, respiratory acidosis, and arterial hypoxemia.
Causes of ventilation respiratory failure:
Inhibition 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, consequences of anoxia of the brain, coma of various etiologies);
Disturbances in the conduction of nerve impulses to the respiratory muscles (due to traumatic injury to the spinal cord, infection such as poliomyelitis, 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 and intensive care units.
Violation of the act of breathing can be observed in trauma or deformation of the chest, pneumothorax, pleural effusion, absence of excursion of the diaphragm.
Ventilatory respiratory failure often occurs in the immediate postoperative period. Factors contributing to ventilation failure include obesity, old age, smoking, cachexia, 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 a reduced, normal or elevated CO2 level in the blood. It develops as a result of damage to the lung tissue, pulmonary edema, severe pneumonia, acid aspiration syndrome and many other causes and leads to severe hypoxemia. The main pathogenetic links of this form of acute respiratory failure are a pulmonary shunt (blood shunt from right to left), a mismatch between ventilation and blood flow, and a violation of diffusion processes.
Causes of parenchymal respiratory insufficiency:
Trauma, sepsis, systemic inflammatory response (released inflammatory mediators: tumor necrosis factor, pro-inflammatory cytokines, thromboxane, NO, arachidonic acid metabolites, impaired oxygen transport when pulmonary functional units are damaged by oxygen radicals passing through the lung filter;
Multiple organ failure syndrome (in these cases, the lungs are usually affected);
Respiratory distress syndrome in adults;
Severe forms of pneumonia;
Pulmonary contusion;
Atelectasis;
Pulmonary edema (caused by increased hydrostatic pressure in the pulmonary capillaries or capillary wall permeability);
Severe form of bronchial asthma;
Pulmonary embolism;
Massive bronchopulmonary aspiration.
Isolation of two forms of acute respiratory failure is arbitrary to a certain extent. Often one form turns into another. A combination of both forms is also possible.
Clinical picture acute respiratory failure can 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 small 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 rises (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 to clear his throat and eliminate bronchial obstruction, then lethargy disappears. Hypercapnia is also characterized by oliguria, which is always observed with severe respiratory acidosis.
Decompensation of the state occurs at the moment when a high level of Pco2 in the blood ceases to stimulate the respiratory center. Signs of decompensation in far advanced cases are a sharp decrease in minute ventilation of the lungs, circulatory disorders and the development of coma, which, with progressive hypercapnia, is CO2 anesthesia. Pco2 in this case reaches 100 mm Hg, but coma can occur even 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 the analysis of arterial blood, indicating a decrease in Po2. it is characterized by a gradual or rapidly progressive course, mild clinical symptoms and the possibility of death in 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 oxygen saturation and 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:
Respiratory disorders (shortness of breath, a gradual decrease in respiratory and minute volumes of breathing, oligopnea, unexpressed cyanosis);
Increasing neurological symptoms (indifference, aggressiveness, agitation, lethargy, coma);
Violations of the cardiovascular system (tachycardia, persistent increase in blood pressure with hypercapnia, decompensation of the cardiovascular system and cardiac arrest).
Clinical signs of acute respiratory failure:
Acute respiratory failure (oligoproe, tachypnea, bradypnea, apnea, abnormal 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 you to make a diagnosis.
Acute heart failure- this is a sudden onset of muscle failure of the ventricles of the heart. This condition can be aggravated by the dissonance between the decrease in the work of one and the normal function of another part of the heart. Sudden onset of heart failure can be fatal.
The causes of acute cardiac dysfunction are myocardial infarction, diffuse myocarditis, excessive exercise, intercurrent infection, as well as other pathological conditions in which hypercatecholaminemia is observed, violation of the ionic composition of the intracellular fluid, conduction disturbance, especially in the atrioventricular system (Morgagni-Edems-Stokes attacks ), impaired 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 minute volume, a sharp decrease in blood supply to the arterial system, is very similar to the picture of acute circulatory vascular insufficiency, therefore it is sometimes referred to as acute cardiac collapse, or cardiogenic shock. Patients have extreme weakness, a condition close to fainting), pallor, cyanosis, cold extremities, very small filling of the pulse. 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, prodiastolic gallop rhythm). At the same time, shortness of breath, swelling of the cervical veins, congestive rales, in the lungs, cyanosis are observed. A sharp slowdown (less than 40 per minute) or an increase (more than 160 per minute) of the pulse is more characteristic of cardiac weakness than vascular weakness. Blood pressure is reduced. There are symptoms of organ ischemia with symptoms of venous plethora due to a 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 trunk of the pulmonary artery or its large branch due to the drift of a blood clot from the veins of the legs, pelvis, less often from the right ventricle or atrium. The patient suddenly develops shortness of breath, cyanosis, sweat, a feeling of pressure or pain in the region of the heart, the pulse becomes very small and frequent, and blood pressure drops. Soon, if the patient remains alive, venous pressure increases, the cervical veins swell, and then the liver enlarges, an accent of II tone on the pulmonary artery and a gallop rhythm are heard. X-ray is determined by an increase in the right ventricle, expansion of the cone of the pulmonary artery. After 1-2 days, signs of a heart attack of pneumonia may appear.
Acute right ventricular failure can be observed in patients with acute myocardial infarction of the posterior wall with concomitant pneumosclerosis and emphysema. Along with the clinic of myocardial infarction, they develop cyanosis, stagnation in the systemic circulation and a sudden enlargement of the liver. Sometimes patients enter the surgical department with a diagnosis of acute abdomen and acute cholecystitis due to the occurrence of 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 upcoming attack of suffocation.
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 mobile 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 region of the heart, shortness of breath, increasing cyanosis, followed by loss of consciousness and the development in most cases of reflex collapse. Prolonged closure of the atrioventricular orifice by a thrombus, as a rule, leads to the death of patients.
Similarly, with mitral stenosis, a syndrome of acute functional insufficiency of the left atrium is often observed. This happens when the defect is compensated by increased work of the left atrium while maintaining the contractile function of the right ventricle. With excessive physical stress, a sudden stagnation of blood in the vessels of the lungs can occur and an attack of cardiac asthma occurs, which can turn into acute pulmonary edema. Sometimes such attacks are repeated often, appear suddenly and just as suddenly disappear, which confirms the great importance of the reflex influence from the atria to the vessels of the lung.
To date, all the mechanisms for the 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 play a big role.
It is known that attacks of cardiac asthma and pulmonary edema can occur when the pulmonary artery receptors are irritated by a cardiac probe during cardiac probing.
With physical exertion, agitation, fever, pregnancy, etc., there is an increased need for oxygen in the body, cardiac activity increases and minute volume increases, which in patients with existing heart lesions can lead to suddenly developing weakness of the left heart. The decompensated difference in the ejection of blood from the right and left parts of the heart leads to an overflow of the small circle, blood circulation. Pathological reflexes due to hemodynamic disorders lead to the fact that the production of glucocorticoids decreases, and mineralocorticoids - increases. This, in turn, enhances vascular permeability, causes sodium and water retention in the body, which further worsens hemodynamic parameters.
It is necessary to take into account another factor that can play an important role in the development of these complications - this is a violation of the lymph circulation in the lung tissue, the expansion of anastomoses between the veins of the large and small circles.
Prolonged increase in capillary pressure in the lungs above 30 mm Hg. Art. causes leakage of fluid 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 capillary pressure is well below 30 mm Hg. Art. Pulmonary edema occurs in patients with a small difference between 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 a pronounced narrowing of the left venous orifice, the development of muscle fibers in the pulmonary arterioles, proliferation of fibrous tissue in the intima of the vessels, thickening of the pulmonary capillaries, hypertrophy of the fibrous base with a partial loss of elasticity of the lung tissue were noted. In this regard, the pulmonary capillaries move away from the alveolar membrane, the alveolar membranes themselves thicken. Such a restructuring begins with an increase in pressure in the pulmonary artery to 50 mm Hg. Art. and higher and most pronounced in the pulmonary vessels with an increase in pulmonary arterial pressure up 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 developing asthma attacks or pulmonary edema. Capillary extravasation is also possible with these changes, but at a higher “critical” level of pulmonary capillary pressure, which is necessary for the occurrence of capillary extravasation and the passage of tissue fluid through the altered alveolar membranes.
Clinic of cardiac asthma and pulmonary edema characterized initially by the occurrence of severe suffocation and severe cyanosis. In the lungs, a large number of scattered dry and wet rales are determined. There is a bubbling breath, a cough with the release of foamy sputum (often stained with blood). Blood pressure is often reduced.
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 detected as one of the manifestations of the syndrome of multiple organ failure.
THE REASONS
All the causes that cause the development of ARF can be divided into three large groups:
1. Extrarenal (extrarenal) causes- lead to a decrease in BCC and a sharp decrease in renal blood flow, which can cause irreversible death of kidney tissue cells. Extrarenal causes of acute renal failure include: severe major surgery, especially in debilitated patients or in elderly patients; injuries accompanied by pain shock and hypovolemia; sepsis; massive blood transfusion; extensive burns; indomitable vomiting; uncontrolled intake of diuretics; cardiac tamponade.
2. Renal (renal) causes- include ischemic and toxic lesions of the renal tissue, acute inflammation of the renal parenchyma or damage to the vessels of the kidneys, which cause necrosis of the renal tissue. The renal causes of acute renal failure include: acute glomerulonephritis; acute tubular necrosis; rheumatic affections of the kidneys; blood diseases; poisoning with salts of mercury, copper, cadmium, poisonous mushrooms, organic fertilizers; malignant arterial hypertension; lupus nephritis; uncontrolled intake of drugs from the group of sulfonamides, anticancer drugs, aminoglycosides, NSAIDs.
3. Subrenal (postrenal) causes- associated with a violation of the outflow of urine, which leads to the accumulation of urine in the pyelocaliceal system, edema and necrosis of renal tissue cells. The renal causes of acute renal failure include: bilateral obstruction of the ureters with calculi, blood clot; urethritis and periurethritis; tumors of the ureters, prostate, bladder; prolonged compression of the ureters in 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 violation of all the functions that the kidneys perform. The loss of the ability of the kidneys to maintain the balance of electrolytes in the blood is accompanied by an increase in the concentration of calcium and potassium and chlorine ions, as well as the accumulation of protein metabolism 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 result of a violation of the excretory function of the kidneys, one of the main symptoms of acute renal failure develops - oliguria (reduction in urine output) up to anuria (complete absence of urine). The condition of patients with acute renal failure is usually moderate or severe, there are disturbances of consciousness (lethargy or excessive excitement), swelling of the extremities, heart rhythm disturbances, nausea and vomiting, an increase in the size of the liver.
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, the duration of which is usually 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 decrease in the volume of urine (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 be extended up to 5-10 days. At the same time, the later ARF developed 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 inhibited, may fall into a coma. Due to the pronounced suppression of immunity, the risk of a secondary infection with the development of pneumonia, stomatitis, parotitis, etc. increases.
3. During the diuretic stage, there is a gradual increase in the volume of urine, reaching about 5 liters of urine per day. The duration of the diuretic stage is usually 10-14 days, during which there is a gradual regression of symptoms of renal failure, restoration of the electrolyte balance of the blood.
4. At the stage of recovery, there is a further restoration of all kidney functions. 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 previous liver disease. The main symptom of acute renal failure is hepatic encephalopathy (HE), which has a decisive influence on the course of acute renal failure and the prognosis of the disease.
One can talk about acute renal failure if encephalopathy develops within 8 weeks from the onset of the first symptoms of acute hepatocellular insufficiency. 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 isolate hyperacute liver failure, which develops within 7 days from the onset of jaundice. Mortality in acute renal failure is, according to different authors, from 50 to 90%.
The main etiological factors in 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 of pregnant women.
The main symptoms and complications of acute renal failure
Hepatic Encephalopathy is a complex of potentially reversible neuropsychiatric disorders resulting from acute or chronic liver failure and/or portosystemic shunting.
According to most researchers, PE develops due to the penetration of endogenous neurotoxins through the blood-brain barrier (BBB) and their effects on astroglia as a result of liver cell deficiency. In addition, the amino acid imbalance that occurs with liver failure affects the development of PE. As a result, the permeability of the BBB, the activity of ion channels changes, neurotransmission and the provision of neurons with macroergic compounds are disturbed. 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 it, as well as with portosystemic shunting of the blood. Ammonia in a non-ionized form (1–3% of the total amount of ammonia in the blood) easily penetrates the BBB, stimulating the transport of aromatic amino acids to 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 the inhibition of neuronal Na +, K + -ATPase and an increase in the transport of aromatic amino acids to 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 a role in the pathogenesis of PE of the inhibitory neurotransmitter g-aminobutyric acid (GABA) of intestinal origin, the excessive intake of which into the brain under conditions of astroglial edema also leads to an increase in neuropsychiatric 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 enhancement of several factors: endogenous neurotoxins, among which ammonia plays a leading role, amino acid imbalance, and changes in the functional activity of neurotransmitters and their receptors.
In the development of encephalopathy in patients with acute renal failure, factors of liver parenchymal insufficiency predominate, the outcome of which is often endogenous hepatic coma. The provoking factors in this case are the increased breakdown of proteins contained in the diet, or when a blood protein enters during gastrointestinal bleeding, inappropriate medication, alcohol excesses, surgical interventions, concomitant infection, etc. Encephalopathy in patients with liver cirrhosis 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 is distinguished .
1. Common symptoms in acute renal failure: nausea, vomiting, anorexia, hyperthermia, malaise and progressive fatigue.
2. Jaundice is a mirror of the degree of liver failure. The level of bilirubin can increase up to 900 µmol/L.
3. "Liver smell" from the mouth (the smell of rotten meat).
4. Flapping tremor. It is determined in patients in the mind. In addition, it can be registered 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 the level of albumin in the blood).
6. Deficiency of coagulation factors due to a decrease in their production by the liver. The number of platelets also decreases. As a result, gastrointestinal bleeding and diapedetic bleeding from the nasopharynx, retroperitoneal space, and injection sites often develop.
7. Metabolic disorders. As a rule, hypoglycemia develops as a result of gluconeogenesis and an increase in insulin levels.
8. Cardiovascular complications:
hyperdynamic circulation (reminiscent of septic shock) - an increase in cardiac index, low peripheral resistance, arterial hypotension;
hypovolemia;
heart enlargement;
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 state is aggravated 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, an increase in the level of blood creatinine. In case of poisoning with acetaminafen, renal failure also develops as a result of the direct toxic effect of the drug. Tubular lesions can develop as a result of hypotension and hypovolemia. The level of blood urea in acute renal failure, as a rule, is low as a result of a decrease in its synthesis in the liver.
Differential diagnosis of acute (fulminant) liver failure should be carried out with bacterial meningitis, brain abscess, encephalitis.
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1. Types of violations of the body's vital functions. Shock, terminal states, acute respiratory, renal, cardiovascular insufficiency in surgical patients.
Shock- an acute critical condition of the body with a progressive insufficiency of the life support system, due to acute circulatory failure, microcirculation and tissue hypoxia.
In shock, the functions of the cardiovascular system, respiration, kidneys change, the processes of microcirculation and metabolism are disturbed. Shock is a polyetiological disease. Depending on the cause of occurrence, the following types are distinguished.
1. Traumatic shock: a) as a result of mechanical trauma (wounds, bone fractures, tissue compression, etc.); b) burn shock (thermal and chemical burns); c) when exposed to low temperature - cold shock; d) as a result of electrical injury - electric shock.
2. Hemorrhagic or hypovolemic shock: a) bleeding, acute blood loss; b) acute violation of the water balance - dehydration of the body.
3. Septic (bacterial-toxic) shock (common purulent processes caused by gram-negative or gram-positive microflora).
4. Anaphylactic shock.
5. Cardiogenic shock (myocardial infarction, acute heart failure)
Varieties and manifestations of terminal states.
Predagonal states;
clinical death.
In addition, grade III-IV shock has a number of signs characteristic of terminal states.
Terminal states most often develop as a result of acute blood loss, traumatic and surgical shock, asphyxia, collapse, severe acute intoxication (sepsis, peritonitis), coronary circulation disorders, etc.
The predagonal state is characterized by a darkened, confused consciousness, pallor of the skin, pronounced acrocyanosis, and circulatory disorders. Eye reflexes are preserved, breathing is weakened, the pulse is thready, blood pressure is not determined. Oxygen starvation and acidosis. In the brain tissue, the amount of free sugar decreases, the content of lactic acid increases. Further development of the pathological process leads to agony.
Agony - consciousness is absent, areflexia, sharp pallor of the skin, pronounced cyanosis. The pulse is only on the carotid arteries, the heart sounds are deaf, bradycardia, breathing is arrhythmic, convulsive. Increasing acidosis, oxygen starvation of vital centers.
clinical death. Respiration and cardiac activity are absent. Exchange processes are kept at the lowest level. The vital activity of the organism is minimal. Clinical death lasts 5-6 minutes (V. A. Negovsky, 1969), but the body can still be revived. First of all, the cerebral cortex dies, as a younger (phylogenetically) formation. Subcortical formations are more resistant and viable.
Biological death develops if measures were not taken in time to revive the body. Irreversible processes develop. The use of revitalization methods are useless.
A comprehensive technique for resuscitation of terminal conditions provides for:
Intra-arterial blood injection;
Heart massage (direct and indirect);
defibrillation of the heart;
Artificial ventilation of the lungs;
Auxiliary artificial circulation.
These activities can be carried out simultaneously, or maybe selectively. It is important to know that if clinical death has occurred, then a complex of therapeutic measures can lead to the revival of the body.
Acute respiratory failure (ARF)- a syndrome based on disturbances in the external respiration system, in which the normal gas composition of arterial blood is not ensured or its maintenance at a normal level is achieved due to excessive functional stress of this system.
Etiology.
Distinguish between pulmonary and extrapulmonary causes of ARF.
Extrapulmonary causes:
1. Violation of the central regulation of respiration: a) acute vascular disorders (acute disorders of cerebral circulation, cerebral edema); b) brain injury; c) intoxication with drugs acting on the respiratory center (narcotic drugs, barbiturates); d) infectious, inflammatory and tumor processes leading to damage to the brain stem; e) coma.
2. Damage to the musculoskeletal apparatus of the chest and damage to the pleura: a) peripheral and central paralysis of the respiratory muscles; b) spontaneous pneumothorax; c) degenerative-dystrophic changes in the respiratory muscles; d) poliomyelitis, tetanus; e) spinal cord injury; f) the consequences of the action of organophosphorus compounds and muscle relaxants.
3.ODN in violation of oxygen transport with large blood loss, acute circulatory failure and poisoning (carbon monoxide).
Pulmonary causes:
1. Obstructive disorders: a) blockage of the respiratory tract by a foreign body, sputum, vomit; b) a mechanical obstruction to the access of air when compressed from the outside (hanging, suffocation); c) allergic laringo - and bronchospasm; d) tumor processes of the respiratory tract; e) violation of the act of swallowing, paralysis of the tongue with its retraction; e) edematous-inflammatory diseases of the bronchial tree.
2. Respiratory disorders: a) infiltration, destruction, degeneration of lung tissue; b) pneumosclerosis.
3. Decreased functioning lung parenchyma: a) lung underdevelopment; b) compression and atelectasis of the lung; c) a large amount of fluid in the pleural cavity; d) pulmonary embolism (PE).
ODN classification.
1. Etiological:
Primary ORF - associated with impaired oxygen delivery to the alveoli.
Secondary ARF - associated with a violation of oxygen transport from the alveoli to the tissues.
Mixed ARF - a combination of arterial hypoxemia with hypercapnia.
2.Pathogenetic:
The ventilatory form of ARF occurs when the respiratory center of any etiology is affected, when the transmission of impulses in the neuromuscular apparatus is disturbed, damage to the chest and lungs, changes in the normal mechanics of breathing in the pathology of the abdominal organs (for example, intestinal paresis).
The parenchymal form of ARF occurs with obstruction, restriction of the airways, as well as in violation of the diffusion of gases and blood flow in the lungs.
The pathogenesis of ARF is due to the development of oxygen starvation of the body as a result of violations of alveolar ventilation, diffusion of gases through the alveolar-capillary membranes and uniform distribution of oxygen throughout organs and systems.
There are three main syndromes of ARF:
I. Hypoxia is a condition that develops as a result of reduced tissue oxygenation.
Taking into account etiological factors, hypoxic conditions are divided into 2 groups:
BUT). Hypoxia due to a reduced partial pressure of oxygen in the inhaled air (exogenous hypoxia), for example, in high altitude conditions.
B) Hypoxia in pathological processes that disrupt the supply of oxygen to tissues at its normal partial voltage in the inhaled air:
Respiratory (respiratory) hypoxia - based on alveolar hypoventilation (impaired airway patency, chest trauma, inflammation and pulmonary edema, respiratory depression of central origin).
Circulatory hypoxia occurs against the background of acute or chronic circulatory failure.
Tissue hypoxia - a violation of the processes of oxygen uptake at the tissue level (potassium cyanide poisoning)
Hemic hypoxia - is based on a significant decrease in erythrocyte mass or a decrease in hemoglobin content in erythrocytes (acute blood loss, anemia).
II. Hypoxemia - a violation of the processes of oxygenation of arterial blood in the lungs. This syndrome can occur as a result of hypoventilation of the alveoli of any etiology (for example, asphyxia), with the predominance of blood flow in the lungs over ventilation with airway obstruction, with impaired diffusion capacity of the alveolar-capillary membrane in respiratory distress syndrome. An integral indicator of hypoxemia is the level of partial oxygen tension in arterial blood (PaO2 is normally 80-100 mm Hg).
III. Hypercapnia - a pathological syndrome characterized by an increased content of carbon dioxide in the blood or at the end of exhalation in the exhaled air. Excessive accumulation of carbon dioxide in the body disrupts the dissociation of oxyhemoglobin, causing hypercatecholaminemia. Carbon dioxide is a natural stimulant of the respiratory center, therefore, at the initial stages, hypercapnia is accompanied by tachypnea, however, as it accumulates excessively in the arterial blood, depression of the respiratory center develops. Clinically, this is manifested by bradypnea and respiratory rhythm disturbances, tachycardia, increased bronchial secretion and blood pressure (BP). In the absence of proper treatment, a coma develops. An integral indicator of hypercapnia is the level of partial tension of carbon dioxide in arterial blood (PaCO2 is normally 35-45 mm Hg).
clinical picture.
Shortness of breath, violation of the rhythm of breathing: tachypne, accompanied by a feeling of lack of air with the participation of auxiliary muscles in the act of breathing, with an increase in hypoxia - bradypnoe, Cheyne-Stokes, Biot breathing, with the development of acidosis - Kussmaul breathing.
Cyanosis: acrocyanosis against the background of pallor of the skin and their normal moisture, with increasing cyanosis becomes diffuse, there may be “red” cyanosis against the background of increased sweating (evidence of hypercapnia), “marbling” of the skin, patchy cyanosis.
In the clinic, there are three stages of ARF.
I stage. The patient is conscious, restless, may be euphoric. Complaints about feeling short of breath. The skin is pale, moist, mild acrocyanosis. The number of breaths (RR) is 25-30 per minute, the number of heartbeats (HR) is 100-110 beats / min, blood pressure is within normal limits or slightly increased, PaO2 is 70 mm Hg, PaCO2 is 35 mm Hg. (hypocapnia is compensatory in nature, as a result of shortness of breath).
II stage. Complaints of severe suffocation. Psychomotor agitation. Delusions, hallucinations, loss of consciousness are possible. The skin is cyanotic, sometimes in combination with hyperemia, profuse sweat. Respiratory rate - 30 - 40 per minute, heart rate - 120-140 beats / min, arterial hypertension. PaO2 decreases to 60 mm Hg, PaCO2 increases to 50 mm Hg.
III stage. Consciousness is absent. Seizures. Expansion of pupils with the absence of their reaction to light, spotted cyanosis. Bradypnoe (RR - 8-10 per minute). Falling BP. Heart rate more than 140 beats / min, arrhythmias. PaO2 decreases to 50 mm Hg, PaCO2 increases to 80 - 90 mm Hg. and more.
Acute heart failure (AHF) is a clinical syndrome resulting from a primary heart disease or other diseases in which the heart does not provide sufficient blood circulation to organs and tissues in accordance with their metabolic needs.
OSN classification.
1. Acute left ventricular failure:
Interstitial pulmonary edema or cardiac asthma:
Alveolar pulmonary edema.
Acute right ventricular failure.
Acute biventricular insufficiency.
According to the severity, the following stages of AHF are distinguished (Killip classification):
Stage I - no signs of heart failure.
Stage II - mild AHF: there is shortness of breath, moist fine bubbling rales are heard in the lower parts of the lungs.
Stage III - severe AHF: severe shortness of breath, a significant amount of moist rales over the lungs.
Stage IV - a sharp fall in blood pressure (systolic blood pressure less than 90 mm Hg) up to the development of cardiogenic shock. Severe cyanosis, cold skin, clammy sweat, oliguria, blackout.
Etiology of acute left ventricular heart failure:
1. IHD: acute coronary syndrome (protracted anginal attack, painless widespread myocardial ischemia), acute myocardial infarction (AMI).
2. Mitral valve insufficiency caused by detachment of the papillary muscle (with AMI) or detachment of the mitral valve chord (with infective endocarditis or chest trauma).
3. Stenosis of the left atrioventricular opening associated with a tumor in any of the chambers of the heart (most often - left atrial myxoma), thrombosis of the mitral valve prosthesis, mitral valve damage in infective endocarditis.
4. Insufficiency of the aortic valve in case of rupture of the aortic valves, with exfoliating aneurysm of the ascending aorta.
5. Acutely increased heart failure in patients suffering from chronic heart failure (acquired or congenital heart defects, cardiomyopathy, post-infarction or atherosclerotic cardiosclerosis); this may be due to hypertensive crisis, paroxysmal arrhythmias, fluid volume overload resulting from inadequate diuretic or excessive fluid therapy.
Etiology of acute right ventricular heart failure:
1.AMI of the right ventricle.
2. Pulmonary embolism (PE).
3. Stenosing process in the right atrioventricular orifice (as a result of a tumor or vegetative growths in infective endocarditis of the tricuspid valve).
4.Asthmatic status.
Etiology of acute biventricular heart failure:
1.AMI with damage to the right and left ventricles.
2. Rupture of the interventricular septum in AMI.
3. Paroxysmal tachycardia.
4. Acute severe myocarditis.
Pathogenesis. Main development mechanisms:
Primary myocardial damage, leading to a decrease in myocardial contractility (CHD, myocarditis).
Pressure overload of the left ventricle (arterial hypertension, aortic valve stenosis).
Left ventricular volume overload (aortic and mitral valve insufficiency, ventricular septal defect).
Decreased filling of the ventricles of the heart (cardiomyopathy, hypertension, pericarditis).
High cardiac output (thyrotoxicosis, severe anemia, cirrhosis of the liver).
Acute left ventricular heart failure.
The main pathogenetic factor is a decrease in the contractility of the left ventricle with preserved or increased venous return, which leads to an increase in hydrostatic pressure in the pulmonary circulation system. With an increase in hydrostatic pressure in the pulmonary capillaries more than 25 - 30 mm Hg. there is an extravasation of the liquid part of the blood into the interstitial space of the lung tissue, which causes the development of interstitial edema. One of the important pathogenetic mechanisms is the foaming of the fluid that has entered the alveoli with each breath, which rises up, filling the bronchi of a larger caliber, i.e. alveolar pulmonary edema develops. So, from 100 ml of sweated plasma, 1 - 1.5 liters of foam is formed. Foam not only disrupts the airway, but also destroys the surfactant of the alveoli, which causes a decrease in lung compliance, increases hypoxia and edema.
Clinical picture:
Cardiac asthma (interstitial pulmonary edema) most often develops at night with a feeling of lack of air, dry cough. The patient is in a forced orthopnea position. Cyanosis and pallor of the skin, cold clammy sweat. Tachypnea, moist rales in the lower parts of the lungs, muffled heart sounds, tachycardia, accent of the second tone over the pulmonary artery.
Alveolar pulmonary edema is characterized by the development of a sharp attack of suffocation, a cough appears with the release of foamy pink sputum, "gurgling" in the chest, acrocyanosis, profuse sweating, tachypnea. In the lungs, mixed moist rales. Tachycardia, accent of the second tone over the pulmonary artery.
Acute right ventricular heart failure is the result of a sharp increase in pressure in the pulmonary artery system. Given the low prevalence of isolated right ventricular AMI and infectious lesions of the tricuspid valve, as a rule, in clinical practice, acute right ventricular failure occurs in combination with left ventricular failure.
Clinical picture: gray cyanosis, tachypnea, acute enlargement of the liver, pain in the right hypochondrium, swelling of the jugular veins, peripheral and abdominal edema.
Acute biventricular heart failure: symptoms of left and right ventricular failure appear simultaneously.
Acute renal failure (ARF) - pathological clinical syndrome of various etiologies, characterized by a significant and rapid decrease in glomerular filtration rate (GFR), which is based on acute damage to the nephron, followed by a violation of its main functions (urinary and urinary) and the occurrence of azotemia, a violation of the acid-base state and water-electrolyte metabolism .
Classification opn.
1. According to the place of occurrence of "damage":
prerenal;
Renal;
Postrenal.
2. By etiology:
Shock kidney - traumatic, hemorrhagic, blood transfusion, septic, anaphylactic, cardiogenic, burn, surgical shock, electrical injury, abortion, postpartum sepsis, severe preeclampsia, dehydration;
Toxic kidney - poisoning with exogenous poisons;
severe infections;
Acute obstruction of the urinary tract;
arenal state.
3.Downstream:
Initial period (period of initial action of factors);
The period of oligo-, anuria (uremia);
Diuresis recovery period:
phase of initial diuresis (diuresis 500 ml/day);
phase of polyuria (diuresis more than 1800 ml / day);
recovery period.
4. By severity:
Grade I - mild: an increase in blood creatinine by 2-3 times;
II degree - moderate: blood creatinine increased by 4-5 times;
Grade III - severe: blood creatinine increased by more than 6 times.
Reasons for the development of the prerenal form of acute renal failure.
1. Decreased cardiac output:
Cardiogenic shock;
Tamponade of the pericardium;
arrhythmias;
Congestive heart failure.
2. Decreased vascular tone:
Anaphylactic, septic shock;
Irrational intake of antihypertensive drugs.
3. Decreased extracellular fluid volume:
bleeding, dehydration,
Profuse vomiting, diarrhea, polyuria.
Reasons for the development of the renal form of acute renal failure.
1. Acute tubular necrosis:
Ischemic;
nephrotoxic;
Drug.
2. Intratubular obstruction:
Pathological cylinders, pigments;
Crystals.
3. Acute tubulointerstitial nephritis:
Drug;
Infectious;
Acute pyelonephritis.
4. Cortical necrosis:
Obstetric;
Anaphylactic shock;
5. Glomerulonephritis.
6. Damage to the renal vessels:
traumatic;
Immunoinflammatory.
Reasons for the development of the postrenal form of acute renal failure.
1. Damage to the ureters:
obstruction (stone, blood clots);
Compression (swelling).
2. Damage to the bladder:
Stones, tumor, inflammatory obstruction, prostate adenoma;
Violation of the innervation of the bladder; spinal cord injury.
3. Urethral stricture.
The pathogenesis is based on a violation of systemic hemodynamics and depletion of the vascular bed of the kidneys. Vasoconstriction is induced with redistribution of blood flow, ischemia of the cortical layer of the kidneys and a decrease in glomerular filtration. The renin - angiotensin - aldosterone system, the production of ADH and catecholamines are activated, which leads to renal vasoconstriction, a further decrease in glomerular filtration, sodium and water retention. If the violation of the blood supply to the kidneys lasts no more than 1-2 hours, their morphological structure is not significantly damaged and functional changes are coming. If renal blood flow is not restored within 1-2 hours, severe morphological changes form in the kidneys. Clinically, this is manifested by a decrease in diuresis (less than 25 ml / hour) and inhibition of the concentration ability of the kidneys (urine density decreases to 1005 - 1008). After 10-12 hours, azotemia and hyperkalemia increase in the blood plasma.
Symptoms of severe hyperkalemia:
Arrhythmias, bradycardia, AV blockade;
paresthesia;
Muscular paralysis;
Oppression of consciousness.
Symptoms of overhydration quickly join oliguria, and especially anuria - peripheral and abdominal edema, pulmonary edema, cerebral edema. The appearance of an excess of underoxidized products in the body contributes to the development of metabolic acidosis, which at the initial stages of the disease is compensated by respiratory alkalosis (shortness of breath). The accumulation of urea and creatinine in conditions of increased protein catabolism and disturbances in the water and electrolyte state increase metabolic acidosis (vomiting). AKI is characterized by hyperphosphatemia with hypocalcemia. In the polyuric phase, hypocalcemia can cause seizures. Severe intoxication is formed, manifested by headache, irritability, anxiety, and then depression of consciousness of varying severity. As acute renal failure progresses, anemia develops, which may be due to blood loss (hemorrhagic syndrome against the background of uremia), shortened life spans and hemolysis of red blood cells, as well as a decrease in the production of erythropoietin by the kidneys. Significant suppression of the immune system contributes to the rapid addition of infectious complications.
2. Shock. Pathogenesis, clinical picture, diagnosis.
In shock, the functions of the cardiovascular system, respiration, kidneys change, the processes of microcirculation and metabolism are disturbed. Shock is a polyetiological disease.
In the development of traumatic shock, the main pathogenetic factors are the pain factor and blood loss (plasma loss), which lead to acute vascular insufficiency with microcirculation disorders and the development of tissue hypoxia.
At the heart of hemorrhagic shock is a decrease in the volume of circulating blood and, as a result, a circulatory disorder. A feature of the pathogenesis of septic shock is that circulatory disturbance under the influence of bacterial toxins leads to the opening of arteriovenous shunts, and blood bypasses the capillary bed, rushing from arterioles to venules. Cell nutrition is disturbed due to a decrease in capillary blood flow and the action of bacterial toxins directly on the cell, the supply of oxygen to the latter is reduced.
1. Burn shock, its features, shock treatment.
Lasts 1-3 days
Occurs with deep burns of more than 15-20% of the body surface.
Consists of 2 phases: erectile and torpid
Erectile phase - the patient is excited, groans, actively complains of pain, A / D is normal or increased.
Torpid phase - lethargy with preserved consciousness, A / D - a tendency to hypotension, reduced CVP, BCC, diuresis. T body N.
The end of the shock period is indicated by the restoration of diuresis.
Septic shock is a state of peripheral vascular collapse caused by endotoxins from Gram-negative, less commonly Gram-positive bacteria.
Clinic. preceded by a progressive bacterial infection; begins with a sharp increase in body temperature to 3940 ° C, chills; intense sweating; shortness of breath, detoxification; a sharp decrease in blood pressure, up to collapse and loss of consciousness.
A syndrome of multiple organ failure develops: cardiovascular disorders: rhythm disturbance, myocardial ischemia, arterial hypotension; respiratory disorders: tachypnea, hypoxia, respiratory distress syndrome; neuropsychiatric disorders: agitation, convulsions, stupor, coma; impaired renal function: oliguria, hyperazotemia, hypercreatininemia; impaired kidney function: jaundice, increased plasma enzyme activity; hemogram changes: thrombocytopenia, anemia, leukocytosis, leukopenia, hypoproteinemia, acidosis; pronounced changes in the hemostasis system - the development of DIC.
There are 3 phases in the development of septic shock: Phase I - early, "warm": fever up to 3840º C, chills; tachycardia; decrease in systolic blood pressure (SAS) to 9585 mm Hg; decrease in diuresis to 30 ml/hour; duration of the phase several hours and depends on the severity of the infection. Phase II - late or "cold": subnormal body temperature; skin is cold, wet; hemorrhages; severe arterial hypotension (CAC decreases to 70 mm Hg); acrocyanosis, tachycardia, thready pulse; impaired skin sensitivity; oliguria, anuria. Phase III - irreversible septic shock: drop in blood pressure; anuria; coma; RDS
Hemotransfusion shock develops only when incompatible blood is transfused through the AB0, Rhesus systems or other acquired systems. With the complete and high-quality conduct of all tests for compatibility, this complication in the practice of a doctor should not be!
Hemotransfusion shock develops only with "negligent attitude to duties" (Art. 172 of the Code of Criminal Procedure of the Russian Federation). Patients with such complications rarely die immediately, so there is always the possibility of saving them. If you conceal an incompatible blood transfusion with a fatal outcome, you will be held criminally liable under Article 103 of the Code of Criminal Procedure of the Russian Federation, and perhaps, by a court decision, and on charges of a more serious CRIME.
Therapeutic measures for transfusion shock should be aimed at: stopping anaphylaxis, cardiovascular insufficiency, eliminating hypovolemia, but the main task is to restore renal blood flow and diuresis, tk. the maximum burden falls on the kidneys to remove the products of hemolysis of erythrocytes, which clog the renal tubules and form renal failure with the development of anuria. They are carried out in the following order
3. First aid for shock. Complex therapy of shock.
In shock, first aid is more effective the sooner it is given. It should be aimed at eliminating the causes of shock (relieving or reducing pain, stopping bleeding, taking measures to improve breathing and cardiac activity and prevent general cooling).
Pain reduction is achieved by giving the patient or injured limb a position in which there are fewer conditions for intensifying pain, by the behavior of reliable immobilization of the injured part of the body, and by giving painkillers.
In case of injury, the bleeding is stopped and the wound is bandaged; in case of bone fractures and extensive damage to soft tissues, splints are applied. The victim must be treated with the utmost respect.
To facilitate breathing, clothes are unbuttoned (unbutton the collar, loosen the belt).
The patient is laid on his back, his head is somewhat lowered, his legs are raised up by 20-30 cm. In this case, the blood flows towards the heart. At the same time, the volume of circulating blood also increases.
To protect against cooling, the patient is covered with blankets: he must not lose his body heat; other means of keeping warm are unacceptable due to the risk of even greater expansion of blood vessels.
In a state of shock, the patient becomes agitated, he is tormented by fear, so the person providing assistance must constantly be there, reassure and do everything to make the patient feel safe. It is extremely important to protect the patient from noise, for example, conversations of other people.
SHOCK TREATMENT
one . Establish an open airway, intubate and mechanically ventilate if necessary.
2. Position patient with legs elevated effectively for hypotension, especially if no medical equipment is available, however, may impair ventilation and, in cardiogenic shock with pulmonary congestion, also cardiac function.
3 . Place intravascular catheters:
1) to peripheral veins 2 large diameter catheters (better ≥ 1.8 mm [≤ 16 G]), which will allow effective infusion therapy → see below;
2) if necessary, the introduction of many drugs (including catecholamines → see. Below) a catheter into the vena cava; also allows you to monitor central venous pressure (CVP);
3) an arterial catheter (usually a radiation catheter) makes invasive blood pressure monitoring in case of persistent shock or the need for long-term use of catecholamines. Catheterization of the vena cava and arteries should not delay treatment.
four . Apply etiologic treatment → see below and maintain circulatory system and tissue oxygenation at the same time
1) if the patient is receiving antihypertensive drugs → cancel them;
2) in most types of shock, restoration of intravascular volume by intravenous infusion of solutions is of primary importance; the exception is cardiogenic shock with symptoms of blood stasis in the pulmonary circulation. Colloidal solutions (6% or 10% hydroxyethyl starch [HES], 4% gelatin solution, dextran, albumin solution) have not been shown to be more effective at reducing mortality than crystalloid solutions (Ringer's solution, polyelectrolyte solution, 0.9% NaCl), although to correct hypovolemia, a smaller volume of colloid is needed than crystalloids. Initially, 1000 ml of crystalloids or 300-500 ml of colloids are usually administered over 30 minutes, and this strategy is repeated depending on the effect on blood pressure, CVP and urine output, as well as side effects (symptoms of volume overload). For massive infusions, do not apply 0.9% NaCl alone, as infusion of large volumes of this solution (incorrectly called saline) results in hyperchloremic acidosis, hypernatremia, and hyperosmolarity. Even with hypernatremia, do not apply 5% glucose to restore volemic shock. Colloidal solutions reproduce the intravascular volume - almost completely remain in the vessels (plasma substitutes - gelatin, 5% albumin solution), or remain in the vessels and lead to the transition of water from the extravascular space to the intravascular [plasma volume increasing agents - hydroxyethyl starch [HES], 20% albumin solution, dextrans); solutions of crystalloids equalize the deficit of extracellular fluid (outside and intravascular); glucose solutions increase the volume of total water in the body (external and intracellular fluid). Correction of a significant deficiency of volemia can begin with the infusion of hypertonic solutions, for example, Special mixtures of crystalloids and colloids (so-called. .5% NaCl with 10% HES) as they increase plasma volume better. In patients with severe sepsis or burdened with an increased risk of acute kidney injury, it is better not to use HES especially with a molecular weight ≥ 200 kD and/or a molar substitution > 0.4, an albumin solution can be used instead (however, not in patients after a head injury);
3) if hypotension fails despite infusion of fluids → start continuous IV infusion (preferably via vena cava catheter) of vasoconstrictor catecholamines, norepinephrine (adrenore, norepinephrine tartrate Agetane), usually 1-20 mcg/min (more than 1-2 mcg / kg / min) or adrenaline 0.05-0.5 mcg / kg / min, or dopamine (dopamine Admeda, Dopamine-Darnitsa, Dopamine hydrochloride, dopamine-Health, Dopmin, currently not drug of choice for septic shock) 3-30 mcg/kg/min and apply invasive blood pressure monitoring. For anaphylactic shock, start with an injection of epinephrine 0.5 mg IM into the outer thigh;
4) in patients with low cardiac output despite appropriate flooding (or in overhydration), administer dobutamine (dobutamine Admeda, dobutamine-Zdorovye) 2-20 mcg/kg/min as a continuous IV infusion; if hypotension coexists, a vasoconstrictor drug may be used concomitantly;
5) simultaneously with the treatment described above, use oxygen therapy (maximum oxygenation of hemoglobin increases its supply to tissues; the absolute indication is SaO 2<95%);
6) if, despite the above actions, SvO 2<70%, а гематокрит <30% → примените трансфузию эритроцитарной массы.
5 . The main method of correction of lactic acidosis is etiological treatment and treatment that supports the function of the circulatory system; evaluate the indications for the administration of NaHCO 3 i.v. at pH<7,15 (7,20) или концентрации гидрокарбонатного иона <14 ммоль / л.
6. Monitor vital signs (blood pressure, pulse, respiration), state of consciousness, ECG, SaO 2 , CVP, gasometric parameters (and possibly lactate concentration), natremia and potassium, kidney and liver function parameters; if necessary, cardiac output and wedge pressure in the capillaries of the lungs.
7. Protect the patient from loss of heat and provide the patient with a calm environment.
8. If shock is present:
1) allow bleeding from the gastrointestinal tract and thromboembolic complications (in patients with active bleeding or a high risk of its occurrence, do not use anticoagulant drugs, only mechanical methods);
2) correct hyperglycemia if > 10-11.1 mmol/l) by continuous IV infusion of short-acting insulin, however avoid hypoglycemia; try to keep the glycemic level between 6.7-7.8 mmol/l (120-140 mg/dl) to 10-11.1 mmol/l (180-200 mg/dl).
4. Fainting, collapse, shock. Anti-shock measures.
Fainting is an attack of short-term loss of consciousness due to a temporary violation of cerebral blood flow.
Collapse (from Latin collapsus - fallen) is a life-threatening condition characterized by a drop in blood pressure and a deterioration in the blood supply to vital organs. In humans, it manifests itself as a sharp weakness, pointed facial features, pallor, cold extremities. It occurs with infectious diseases, poisoning, large blood loss, overdose, side effects of certain drugs, etc.
Shock is an acute critical state of the body with progressive insufficiency of the life support system, due to acute circulatory, microcirculation and tissue hypoxia.
Basic anti-shock measures.
Traumatic shock is the body's response to pain stimuli caused by mechanical, chemical or thermal injury.
The frequency and severity of shock increases significantly during a nuclear war. Especially often it will be observed with combined radiation injuries, since the effect of ionizing radiation on the central nervous system disrupts its regular functions. This, in turn, leads to a disruption in the activity of organs and systems, i.e. to metabolic disorders, a drop in blood pressure, which predisposes to the appearance of shock.
Depending on the reasons that led to the shock, there are:
one). Traumatic shock caused by various injuries,
2). Burn shock that occurs after a burn injury,
3). Operational shock caused by surgery with insufficient anesthesia,