Critical disability in surgical patients. Specialized secondary education of medical profile Disability syndromes

CRITICAL IMPAIRMENTS IN SURGICAL PATIENTS R.T. Majidov

Comatose states

Alcohol intoxication
Skull trauma
Poisoning with medicinal products
Meningitis, encephalitis
Uremia and other metabolic disorders
Diabetes
Brain hypoxia
Epilepsy

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

Open eye
State of speech
Physical activity
the best indicator is 15
worst indicator - 3

The stages of the breathing process

External respiration
Transport function of blood
Tissue respiration (consumption of O2 and ex.
CO2)

Lung volumes and capacities

Respiratory volume
Spare
volume
inhalation
Spare
volume
exhalation
Residual volume
Total capacity
Vital capacity
Inspiratory capacity
Functional
residual capacity

Parenchymal mechanism of pulmonary gas exchange disorder

Healing activities
Oxygen therapy
(insufflation
humidified oxygen): through a catheter,
hermetic masks, through the tent
Recovery
free
passability
bronchi:
expectorant
funds,
reducing the viscosity of mucus, ensuring
deep breath, cough stimulation, cleansing
bronchial tree
Expansion of the lung

The ventilation mechanism of pulmonary gas exchange disorders

Healing activities
Increased activity of functional mechanisms
Providing spontaneous ventilation
Temporary replacement of spontaneous breathing with mechanical ventilation
We reach by:
Mobilizing lung reserves
Elimination of acidosis and alkalosis
Improving respiratory muscle function
Respiratory center excitation
Mechanical ventilation
Hyperbaric oxygenation

Types of acute respiratory failure

Pulmonary edema
Asmatic
state
Total
bronchospasm
Electrical trauma
Epileptic
status
Aspiration
pneumonitis
Drowning
(aspiration)
Strangulation
asphyxia (suicidal
attempt)
Tetanus
Botulism

Indicators of the mechanisms of hemodynamics

Blood pressure
Minute blood circulation
Central venous pressure
Circulating blood volume

Clinical syndrome of circulatory disorders

Heart failure
Circulatory failure
Primary and secondary stop
hearts

Causes of primary cardiac arrest

Cardiac genesis
Heart attack
myocardium,
break
aneurysms
hearts,
coronary
embolism,
occlusion
intracardiac
blood flow, cardiac fibrillation
Extra-heart genesis
Reflex cardiac arrest
Cardiac arrest during anesthesia
Electrical trauma
Due to
acute deficiency of OCC (bleeding,
collapse)
Citrate cardiac arrest
Asphyxia, drowning, intoxication

Cardiac arrest options

Stopping a healthy heart
Stop
"potentially
hearts "
Stopping a sick heart
healthy

Clinic of acute cardiac arrest

Sudden deterioration in general condition
Loss of consciousness, convulsions
Breathing disorder, areflexia
Disappearance of pulse, heart beat,
heart tones
The fall blood pressure

Forms of circulatory failure

Cardiac
Vascular
Peripheral
Cardiogenic
Hypovolemic
Metabolic

Forms of acute circulatory disorders

Embolism pulmonary artery
Myocardial infarction
Hypertensive crisis
Diabetic coma

Syndromes of disorders of water and electrolyte balance

Syndromes of disorders of water electrolyte balance
Dehydration
Water
intoxication
Hyponatremia
Hypernatremia
Hypokalemia
Hyperkalemia

Acid-base balance syndromes

Metabolic acidosis
Respiratory acidosis
Metabolic alkalosis
Respiratory alkalosis

Types of shock

Hemorrhagic shock
Traumatic shock
Toxic-infectious shock
Anaphylactic shock

Types of critical conditions

Liver failure
Renal failure
Hemocoagulation syndromes
Pulmonary embolism

Metabolic functions in critical conditions and their correction

BX
Energy exchange
Protein, fat and carbohydrate metabolism
Clinical
Aspects
pathology
metabolism

Parenteral nutrition

Parenteral nutrition preparations: amino acid
reserves, fat emulsions, carbohydrates, electrolyte
solutions, vitamins, anabolic hormones
Monitoring homeostasis indicators
Complications of parenteral nutrition:
related to central venous catheterization technique
associated with a long stay of the catheter in
central vein
septic complications
metabolic
disorders
related
with
the introduction of various solutions
pyrogenic reactions
fat embolism
air embolism

Terminal state

Pre-gonal state
Agonal state
Clinical death
The initial stages of resuscitation
period

1. Types of disorders of the body. Shock, terminal conditions, acute respiratory, renal, cardiovascular failure in surgical patients.

Shock - an acutely emerging critical state of the body with progressive failure of the life support system, caused by acute insufficiency of blood circulation, microcirculation and tissue hypoxia.

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

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

2. Hemorrhagic, or hypovolemic, shock: a) bleeding, acute blood loss; b) acute water imbalance - 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 conditions.

Pre-gonal states;

Clinical death.

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

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

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

Agony - there is no consciousness, areflexia, severe pallor of the skin, pronounced cyanosis. Pulse only on carotid arteries, deaf heart sounds, bradycardia, arrhythmic breathing, convulsive. Increasing acidosis, oxygen starvation of vital centers.

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

Biological death develops if measures were not taken in time to revive the body. Irreversible processes develop. Reanimation techniques are useless.

A comprehensive technique for resuscitation of terminal conditions provides for:

Intra-arterial blood pressure;

Heart massage (direct and indirect);

Defibrillation of the heart;

Artificial ventilation of the lungs;

Assisted artificial circulation.

These activities can be carried out simultaneously, and maybe selectively. It is important to know what if it has come clinical death, then a complex of therapeutic measures can lead to the revitalization of the body.

Acute Respiratory Failure (ARF) - a syndrome based on disorders in the system external respirationin which the normal gas composition of arterial blood is not provided 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 neoplastic processes leading to damage to the brain stem; e) coma.

2. Damage to the musculoskeletal system 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. ONE in violation of oxygen transport with large blood loss, acute failure circulation and poisoning (carbon monoxide).

Pulmonary causes:

1.Obstructive disorders: a) blockage respiratory tract foreign body, sputum, vomit; b) mechanical obstruction to air access when compressed from the outside (hanging, strangulation); c) allergic laryngo - and bronchospasm; d) neoplastic 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.

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

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

ODN classification.

1.Etiological:

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

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

Mixed ODN - a combination of arterial hypoxemia with hypercapnia.

2.Pathogenetic:

The ventilation form of ODN occurs when the respiratory center of any etiology is damaged, when impulse transmission in the neuromuscular apparatus is disturbed, chest and lung injuries, changes in the normal mechanics of respiration in case of organ pathology abdominal cavity (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.

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

There are three main ADF syndromes:

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:

AND). Hypoxia due to low oxygen partial pressure 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 stress in the inhaled air:

Respiratory (respiratory) hypoxia - the basis is 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 - a violation of the processes of oxygen uptake at the tissue level (poisoning with potassium cyanide)

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

II.Hypoxemia - 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 a predominance of blood flow in the lungs over ventilation in case of airway obstruction, in case of impaired diffusion capacity of the alveolar-capillary membrane in respiratory distress syndrome. An integral indicator of hypoxemia is the level of partial tension of oxygen in arterial blood (PaO2 is normally 80-100 mm Hg).

III.Hypercapnia is a pathological syndrome characterized by increased content 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 its excessive accumulation in arterial blood, depression of the respiratory center develops. Clinically, this is manifested by bradypne and respiratory rhythm disturbances, tachycardia, increased bronchial secretion and blood pressure (BP). In the absence of proper treatment, it develops coma... An integral indicator of hypercapnia is the level of partial tension of carbon dioxide in arterial blood (PaCO2 is 35-45 mm Hg in the norm).

The clinical picture.

Shortness of breath, disturbance in the rhythm of breathing: tachypnoe, 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, Biota breathing, with the development of acidosis - breathing of Kussmaul.

Cyanosis: acrocyanosis against the background of pallor of the skin and their normal moisture, with an increase in cyanosis becomes diffuse, there may be "red" cyanosis against the background excessive sweating (evidence of hypercapnia), "marbling" of the skin, spotted cyanosis.

In the clinic, there are three stages of ODN.

Stage I. The patient is conscious, restless, and may be euphoric. Complaints about feeling short of breath. The skin is pale, moist, mild acrocyanosis. The number of breaths (BH) 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 70 mm Hg, PaCO2 35 mm Hg. (hypocapnia is compensatory in nature as a result of shortness of breath).

Stage II. Complaints of severe suffocation. Psychomotor agitation. Delirium, hallucinations, 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. PaO2 decreases to 60 mm Hg, PaCO2 increases to 50 mm Hg.

Stage III. There is no consciousness. Convulsions. Dilatation of the pupils with the absence of their reaction to light, spotted cyanosis. Bradypnoe (BH - 8-10 per minute). Falling blood pressure. 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) - this clinical syndromeresulting from primary disease heart 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.

In terms of severity, the following stages of AHF are distinguished (Killip's 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, over the lungs a significant amount of moist wheezing.

Stage IV - a sharp drop in blood pressure (systolic blood pressure of 90 mm Hg or less) until the development of cardiogenic shock. Severe cyanosis, cold skin, clammy sweat, oliguria, darkening of consciousness.

Etiology of acute left ventricular heart failure:

1.IHD: acute coronary syndrome (prolonged anginal attack, painless widespread myocardial ischemia), acute heart attack myocardium (AMI).

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

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

4.Insufficiency aortic valve with rupture of the valves of the aorta, with dissecting aneurysm of the ascending aorta.

5.Acutely increased heart failure in patients with chronic heart failure (acquired or congenital defects heart, cardiomyopathy, postinfarction or atherosclerotic cardiosclerosis); this may be associated with hypertensive crisis, arrhythmia paroxysm, fluid overload as a result of inadequate diuretic or excessive fluid therapy.

Etiology of acute right ventricular heart failure:

1. AMI of the right ventricle.

2.Pulmonary embolism (PE).

3.Stenotic process in the right atrioventricular orifice (as a result of a tumor or vegetative growths with 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 myocarditis of severe course.

Pathogenesis. Basic development mechanisms:

Primary myocardial damage, leading to a decrease in myocardial contractility (coronary artery disease, myocarditis).

Left ventricular pressure overload (arterial hypertension, aortic valve stenosis).

Overload of the left ventricle volume (insufficiency of the aortic and mitral valves, defect of the interventricular septum).

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

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

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 system of the pulmonary circulation. With an increase in hydrostatic pressure in the pulmonary capillaries of more than 25 - 30 mm Hg. transudation of the liquid part of the blood into the interstitial space of the lung tissue occurs, which causes the development of interstitial edema. One of the important pathogenetic mechanisms is foaming at each inhalation of the fluid that has entered the alveoli, which rises upward, 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, this 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 shortness of breath, dry cough. A patient in a forced orthopnea position. Cyanosis and pallor of the skin, cold clammy sweat. Tachypnea, moist rales in the lower 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, there is a cough with pink foamy sputum, "bubbling" in the chest, acrocyanosis, profuse sweating, tachypnea. Lungs of various sizes, moist rales. Tachycardia, accent of the second tone over the pulmonary artery.

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

Clinical picture: gray cyanosis, tachypnoe, acute liver enlargement, pain in the right hypochondrium, swelling of the cervical veins, peripheral and cavity 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 the 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 location of the "damage":

Prerenal;

Renal;

Post-renal.

2.By etiology:

Shock kidney - traumatic, hemorrhagic, blood transfusion, septic, anaphylactic, cardiogenic, burn, operational shock, electrical trauma, termination of pregnancy, postpartum sepsis, severe gestosis, dehydration;

Toxic kidney - poisoning with exogenous poisons;

Severe infections;

Acute obstruction urinary tract;

Arenal condition.

3.With the flow:

Initial period (period of the initial action of factors);

The period of oligo -, anuria (uremia);

Diuresis recovery period:

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

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

recovery period.

4.By severity:

I degree - mild: an increase in the content of blood creatinine in 2-3 times;

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

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

The reasons for the development of prerenal ARF.

1.Decrease cardiac output:

Cardiogenic shock;

Pericardial tamponade;

Arrhythmias;

Congestive heart failure.

2.Reduction of vascular tone:

Anaphylactic, septic shock;

Irrational intake of antihypertensive drugs.

3.Reduction of extracellular fluid volume:

Blood loss, dehydration,

Profuse vomiting, diarrhea, polyuria.

The reasons for the development of the renal form of ARF.

1.Acute tubular necrosis:

Ischemic;

Nephrotoxic;

Drug.

2.Internal obstruction:

Pathological cylinders, pigments;

Crystals.

3.Acute tubulo-interstitial 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 postrenal ARF.

1. Damage to the ureters:

Obstruction (stone, blood clots);

Compression (swelling).

2.Loss bladder:

Stones, swelling, inflammatory obstruction, prostate adenoma;

Disruption 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 a redistribution of blood flow, ischemia of the renal cortex and a decrease in glomerular filtration. Renin - angiotensin - aldosterone system, production of ADH and catecholamines are activated, which leads to renal vasoconstriction, further decrease in glomerular filtration, sodium and water retention. If the violation of the blood supply to the kidneys lasts no more than 1-2 hours, their morphological structure is not significantly damaged and functional changes are of an incoming nature. If renal blood flow is not restored within 1-2 hours, severe morphological changes form in the kidneys. Clinically, this is manifested by a decrease in urine output (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 blood plasma.

Symptoms of severe hyperkalemia:

Arrhythmias, bradycardia, AV - blockade;

Paresthesia;

Muscle paralysis;

Depression of consciousness.

To oliguria, and especially anuria, symptoms of overhydration quickly join - peripheral and cavity edema, pulmonary edema, cerebral edema. The appearance of an excess of under-oxidized products in the body contributes to the development of metabolic acidosis, which in 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-electrolyte state increase metabolic acidosis (vomiting). ARF 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 ARF progresses, anemia develops, which may be due to blood loss ( hemorrhagic syndrome against the background of uremia), a reduction in the life span and hemolysis of erythrocytes, as well as a decrease in the production of erythropoietin by the kidneys. A significant suppression of the immune system contributes to the rapid addition of infectious complications.

2. Shock. Pathogenesis, clinical picture, diagnostics.

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

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

At the heart of hemorrhagic shock there 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 impaired blood circulation under the influence of bacterial toxins leads to the opening of arteriovenous shunts, and the blood bypasses the capillary bed, rushing from arterioles to venules. Cell nutrition is disrupted due to a decrease in capillary blood flow and the action of bacterial toxins directly on the cell, the supply of the latter with oxygen decreases.

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 agitated, groans, actively complains of pain, A / D is normal or increased.

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

The end of the period of shock is evidenced by the restoration of diuresis

Septic shock is a condition of peripheral vascular collapse caused by endotoxins from gram-negative bacteria, less often by endotoxins from gram-positive bacteria.

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

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

There are 3 phases of the development of septic shock: Phase I - early, "warm": an increase in body temperature to 3840 ° C, chills; tachycardia; a decrease in systolic blood pressure (SAS) to 9585 mm Hg; a decrease in urine output to 30 ml / hour; the duration of the phase several hours and depends on the severity of the infection. Phase II - late or "cold": subnormal body temperature; cold, moist skin; hemorrhages; severe arterial hypotension (CAS decreases to 70 mm Hg); acrocyanosis, tachycardia, thread-like pulse; skin sensitivity disorder; oliguria, anuria. Phase III - irreversible septic shock: drop in blood pressure; anuria; coma; RDS

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

Hemotransfusion shock develops only with "negligent attitude to duties" (Art. 172 of the Criminal Procedure Code of the Russian Federation). Patients with such complications rarely die immediately, so there is always an opportunity to save them. If you conceal an incompatible fatal blood transfusion, 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 blood transfusion shock should be aimed at: relieving anaphylaxis, cardiovascular failure, eliminating hypovolemia, but the main task is to restore renal blood flow and urine output, because the maximum load on the kidneys is 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 health care in shock. Complex therapy shock.

In shock, first aid is the more effective, the earlier it is provided. 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 pain intensification, by the behavior of reliable immobilization of the injured part of the body, by giving painkillers.

When injured, the bleeding is stopped and the wound is bandaged; for bone fractures and extensive damage to soft tissues, splints are applied. The victim should be treated as carefully as possible.

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

The patient is placed on his back, the head is somewhat lowered, the legs are raised upward 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 from cooling, the patient is covered with blankets: he should not lose the heat of his body; other means of keeping warm are unacceptable due to the danger of further dilation of blood vessels.

In a state of shock, the patient becomes agitated, he is tormented by fear, therefore, the person providing assistance must constantly be there, calm down and do everything to make the patient feel safe. It is imperative to protect the patient from noise, such as conversations with people around him.

SHOCK TREATMENT

one . Provide an airway, if necessary, intubate and mechanically ventilate the lungs.

2. Position the patient with raised legs effectively in case of hypotension, especially if no medical equipment is available, however, it can impair ventilation, and in cardiogenic shock with stagnation of blood in the pulmonary circulation - also the work of the heart.

3. Place intravascular catheters:

1) up to peripheral veins 2 catheters of large diameter (preferably ≥ 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 in the vena cava; also allows you to monitor central venous pressure (CVP);

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

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

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

2) in most types of shock, the restoration of intravascular volume by intravascular infusion of solutions is of primary importance; the exception is cardiogenic shock with symptoms of stagnation of blood in the pulmonary circulation. It has not been proven that colloidal solutions (6% or 10% hydroxyethyl starch [HES] solution, 4% gelatin solution, dextran, albumin solution) reduce mortality more effectively than crystalloid solutions (Ringer's solution, polyelectrolyte solution, 0.9% NaCl), although to correct hypovolemia, a smaller volume of colloid is needed than crystalloids. At the beginning, usually 1000 ml of crystalloids or 300-500 ml of colloids are injected for 30 minutes, and this strategy is repeated depending on the effect on blood pressure, CVP and diuresis, as well as side effects (symptoms of volume overload). For massive infusions, do not apply 0.9% NaCl exclusively, as infusion of large volumes of this solution (which is incorrectly called physiological) results in hyperchloremic acidosis, hypernatremia and hyperosmolarity. Even with hypernatremia, do not apply 5% glucose to restore volemia in shock. Colloidal solutions reproduce the intravascular volume - they almost completely remain in the vessels (plasma-substituting agents - gelatin, 5% albumin solution), or remain in the vessels and lead to the transfer of water from the extravascular space to the intravascular [means that increase the plasma volume - hydroxyethylated starch [HES], 20% solution of albumin, dextran); crystalloid solutions equalize the deficiency of extracellular fluid (extra- and intravascular); glucose solutions increase the volume of total water in the body (external and intracellular fluid). Correction of a significant deficit of volemia can begin with the infusion of hypertonic solutions, for example, Special mixtures of crystalloids and colloids (so-called resuscitation in small volumes with the use between others. 7 , 5% NaCl with 10% HES) as they increase the plasma volume better. In patients with severe sepsis or at increased risk acute injury renal better not use HES, especially those with a molecular weight ≥ 200 kDa and / or molar displacement\u003e 0.4, albumin solution may be used instead (but not in patients with head injury);

3) if it is not possible to eliminate hypotension, despite the infusion of solutions → start a constant intravenous infusion (preferably through a catheter into the vena cava) of catecholamines, vasoconstrictor, norepinephrine (adrenore, noradrenaline tartrate Agetan), usually 1-20 μg / min (more than 1-2 μg / kg / min) or epinephrine 0.05-0.5 μg / kg / min, or dopamine (dopamine Admeda, Dopamine-Darnitsa, Dopamine hydrochloride, dopamine-Health, Dopmin, at the moment is not drug of choice for septic shock) 3-30 mcg / kg / min and use 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 the corresponding floods (or in hyperhydration), inject dobutamine (dobutamine Admed, dobutamine-Health) 2-20 μg / kg / min in a constant intravenous infusion; if hypotension coexists, a vasoconstrictor drug can be used simultaneously;

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

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

five . The main method for correcting lactic acidosis is etiological treatment and treatment that maintains the function of the circulatory system; evaluate the indications for the introduction 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, gas metrics (and possibly lactate concentration), natremia and potassium, kidney and liver function parameters; if necessary, cardiac output and pulmonary capillary wedge pressure.

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

8. If the shock contains:

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\u003e 10-11.1 mmol / L) constant intravenous infusion of short-acting insulin, but avoid hypoglycemia; try to maintain a 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 caused by temporary disturbance of cerebral blood flow.

Collapse (from Lat. 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 is manifested by severe 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 acutely emerging critical state of the body with progressive failure of the life support system, caused by acute insufficiency of blood circulation, microcirculation and tissue hypoxia.

The main anti-shock measures.

Traumatic shock is the body's response to painful irritations caused by mechanical, chemical or thermal trauma.

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 disruption of the activity of organs and systems, i.e. to metabolic disorders, a drop in blood pressure, which predisposes to 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 pain relief

LEARNING LESSON PLAN No. 40

the date according to the calendar-thematic plan

Groups: General Medicine

Discipline: Surgery with the basics of trauma

Number of hours: 2

Lesson topic:

Type of training session: lesson of learning new teaching material

Type of training session: lecture

The objectives of training, development and education: formation of knowledge about the main stages of dying, the procedure for carrying out resuscitation measures; idea of \u200b\u200bpostresuscitation illness;

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

Training: on the specified topic.

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

Education: 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 must: know the main stages of dying, their clinical symptoms, the procedure for carrying out resuscitation measures; have an idea of \u200b\u200bpostresuscitation illness.

Material and technical support of the training session: presentation, situational tasks, tests

LESSON PROCESS

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, in polls(sequence and methods of presentation):

Securing the material : solving situational problems, test control

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

Home assignment: 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 year

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

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 structure, 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, sterilization by healthcare institutions

Teacher: L.G. Lagodich

LECTURE OUTLINE

Lecture topic: General disorders of the body 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 conducting resuscitation measures, performance criteria. Conditions for terminating resuscitation measures.

3. Postresuscitation illness. Organization of observation and patient care. Biological death. Death statement.

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, which are based on the increasing hypoxia of all tissues (primarily the brain), acidosis and intoxication with products of impaired metabolism.

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

Terminal states include:

Severe shock (shock grade IV)

Transcendental coma

Collapse

Preagonal state

Terminal pause

Agony

Clinical death

Terminal states in their development have3 stages:

1. Preagonal state;

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

2. Agonal state;

3. Clinical death.

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

Normal dying, so to speak, consists of several stages, successively replacing each otherDying stages:

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

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

3. The next step in 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 a person is considered dead. However, the tissues retain minimal metabolic processes that support 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 respiration and blood circulation. Under normal room conditions, the duration of this period is 6-8 minutes, which is determined by the time during which it is possible to fully restore the functions of the cerebral cortex.

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

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

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

The distinction between clinical death (a reversible stage of dying) and biological death (an irreversible stage of dying) was decisive for the formation of resuscitation - a science that studies the mechanisms of dying and reviving a dying organism. The term "resuscitation" itself was first introduced in 1961 by VA Negovsky at the international congress of traumatologists in Budapest. Anima is the soul, re is the reverse action, thus reanimation is the violent return of the soul to the body.

The formation of intensive care medicine in the 60s and 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 technique of mechanical ventilation. Direct and indirect heart massage. Criteria for the effectiveness of resuscitation measures.

Artificial respiration (artificial lung ventilation - mechanical ventilation). The 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 measure of first aid for drowned persons, in case of suffocation (asphyxia when hanging), electric shock, heat and sunstroke, with some poisoning. In the case of clinical death, i.e. in the absence of spontaneous breathing and heartbeat, artificial respiration is performed simultaneously with heart massage. The duration of artificial respiration depends on the severity of respiratory distress, and it should be continued until completely spontaneous breathing is restored. If there are obvious signs of death, such as cadaver spots, 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 blow the patient up to 1000-1500 ml of fresh air for each breath. But non-specialists certainly do not have such devices at hand. The old methods of artificial respiration (Sylvester, Schaeffer, etc.), which are based on various techniques of chest compression, turned out to be insufficiently effective, since, firstly, they do not ensure the release of the airways from the sunken tongue, and secondly, with with their help, no more than 200-250 ml of air gets into the lungs in 1 breath.

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

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

So, if the patient does not have his own respiratory movements, artificial respiration must be started immediately! If there are doubts whether the victim is breathing or not, it is necessary, without hesitation, to start “breathing for him” and not to waste precious minutes looking for a mirror, putting it to his mouth, etc.

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

1) take a handkerchief or any other piece of fabric (better than gauze);

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

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

4) apply the tissue with a hole on the patient's nose or mouth (depending on the chosen method of I. d.); 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 to 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 cleans the victim's oropharynx of vomit. If the victim's jaws are tightly compressed, the rescuer spreads them apart, if necessary, using a mouth expander tool.

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

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

Once sealed, the rescuer exhales quickly, forcefully, blowing air into the patient's respiratory tract 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, then the volume of the blown air is small or the tongue sinks.

After the end of the exhalation, the rescuer unbends and frees 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-fledged independent exhalation. The patient's exhalation should last about 2 seconds, in any case, it is better that it was twice as long as the inhalation. In a pause before the next inhalation, the rescuer needs to make 1-2 small regular inhales - exhalation "for himself." The cycle is repeated first at a frequency of 10-12 per minute.

If a large amount of air enters not the lungs, but the stomach, the bloating of the latter will make it difficult to save the patient. Therefore, it is advisable to periodically release his stomach from the 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 an injury to the lips or jaws. The rescuer, putting one hand on the victim's forehead and the other on his chin, overextens his head and simultaneously presses his lower jaw to the upper one. 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 him. Then the rescuer makes a strong blowing of air through the nostrils (1-1.5 liters), while following the movement of the chest.

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

Artificial respiration should be carried out without interruption for more than 3-4 s, 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 swelling of the patient's chest, no bloating, gradual pinking of the facial skin). Constantly watch that vomit does not appear in the mouth and nasopharynx, and if this happens, you should clear the victim's airways through the mouth with a finger wrapped in a cloth before inhaling again. As the rescuer is undergoing artificial respiration, his head may become dizzy due to a lack of carbon dioxide in his body. Therefore, it is better for two rescuers to blow the air, changing after 2-3 minutes. If this is not possible, then every 2-3 minutes the breaths should be reduced 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 carrying out artificial respiration in a victim with respiratory arrest, it is necessary to check every minute whether he also has cardiac arrest. To do this, you need to periodically probe the pulse on 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, after which they "slide" 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, it is necessary to immediately begin an indirect heart massage, combining it with artificial respiration. If you skip the moment of cardiac arrest and give the patient only artificial respiration without cardiac massage for 1-2 minutes, then, as a rule, it will not be possible to save the victim.

Mechanical ventilation with the help of equipment is a special conversation in practical classes.

Features of artificial respiration in children. To restore breathing in children under 1 year old, artificial lung ventilation is carried out by the mouth-to-mouth and nose method, in children over 1 year old - by the mouth-to-mouth method. Both methods are carried out in the position of the child on his back, for children under 1 year old, a low roller (folded blanket) is placed under the back or the upper body is slightly raised with the hand brought under the back, the child's head is thrown back. The caregiver takes a breath (shallow!), Hermetically covers the mouth and nose of the child, or (in children over 1 year old) only the mouth, and blows air into the child's respiratory tract, the volume of which should be the smaller, the younger the child (for example, in a newborn it is equal to 30-40 ml). When a sufficient amount of air is blown in and air enters the lungs (and not the stomach), chest movements appear. When you finish blowing, you need to make sure that the chest is descending. Injection of an excessively large volume of air 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 inhalation should correspond to the age-related frequency of respiratory movements, which decreases with age. On average, the respiratory rate per minute is in newborns and children up to 4 months. Life - 40, at 4-6 months. - 40-35, at 7 months. - 2 years old - 35-30, at 2-4 years old - 30-25, at 4-6 years old - about 25, at 6-12 years old - 22-20, at 12-15 years old - 20-18.

Heart massage - a method of renewal and artificial maintenance of blood circulation in the body by rhythmic contractions of the heart, which facilitate the movement of blood from its cavities into the great vessels. Applied in cases of sudden cessation of cardiac activity.

Indications for cardiac massage are primarily determined by general indications for resuscitation, i.e. in the case when there is even the slightest chance to restore not only independent cardiac activity, but also all other vital functions of the body. Carrying out heart massage is not indicated in the absence of blood circulation in the body for a long time (biological death) and with the development of irreversible changes in organs that cannot be replaced later by transplantation. It is inappropriate to massage the heart if the patient has organ injuries that are clearly incompatible with life (primarily the brain); with precisely and in advance established terminal stages of cancer and some other incurable diseases. There is no need for cardiac massage and when suddenly stopped blood circulation can be restored using electrical defibrillation in the first seconds of ventricular fibrillation, established during monitoring of the patient's heart activity, or by applying a jerky blow to the patient's chest in the area of \u200b\u200bthe projection of the heart in case of a sudden and documented the screen of his asystole cardioscope.

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

Mechanism of actiondirect heart massage lies in the fact that when the heart is compressed, the blood in its cavities flows from the right ventricle into the pulmonary trunk and, while artificial ventilation is carried out, is saturated with oxygen in the lungs and returns to the left atrium and left ventricle; from the left ventricle, oxygenated blood enters the systemic circulation, and therefore to the brain and heart. As a result of this restoration of the energy resources of the myocardium, it is possible to resume the contractile ability of the heart and its independent activity when the blood circulation stops as a result of asystole of the ventricles of the heart, as well as fibrillation of the ventricles of the heart, which is successfully eliminated.

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

Direct heart massage is often more effective than indirect, because allows you to directly monitor the state of the heart, feel the tone of the myocardium and promptly eliminate its atony by injecting intracardiac solutions of adrenaline or calcium chloride without damaging the branches of the coronary arteries, since it is possible to visually select the avascular area of \u200b\u200bthe heart. Nevertheless, with the exception of a few situations (for example, multiple rib fractures, massive blood loss and the inability to quickly eliminate hypovolemia - an "empty" heart), indirect massage should be preferred, because for thoracotomy, even in the operating room, certain conditions and time are required, and the time factor in resuscitation is decisive. An indirect cardiac massage can be started almost immediately after the detection of circulatory arrest and can be performed by any previously trained person.

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

Constriction of the pupils

And the emergence of independent breaths.

The effectiveness of 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 is immediately above the xiphoid process).

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

Monitoring the effectiveness of chest compressions carried out constantly in the course of its implementation. To do this, lift the upper eyelid of the patient with a finger and monitor the width of the pupil. If, within 60-90 s of carrying out a heart 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 conducting a heart massage are strictly followed, to resort to drug elimination of myocardial atony or go (subject to conditions) to direct heart massage.

When signs of the effectiveness of chest compressions appear, but there is no tendency to restore independent cardiac activity, one should assume the presence of ventricular fibrillation, which is specified using electrocardiography. According to the picture of fibrillation oscillations, the stage of ventricular fibrillation of the heart is determined and indications for defibrillation are established, which should be as early as possible, but not premature.

Failure to follow the rules of chest compressions can lead to complications such as fractured ribs, development of pneumo- and hemothorax, liver rupture, etc.

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

3. Postresuscitation illness. Organization of observation and patient care. Biological death. Death statement.

In the case of the effectiveness of the resuscitation measures and the patient, spontaneous breathing and heart contractions are restored. He enters the periodpostresuscitation disease.

Postresuscitation period.

In the postresuscitation period, several stages are distinguished:

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

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

3. Stage of normalization of functions.

Biological death. Death statement.

Biological death (or true death) is an irreversible cessation of physiological processes in cells and tissues. Irreversible termination is usually understood as “irreversible in the framework of modern medical technologies” termination of processes. Over time, the possibilities of medicine to resuscitate deceased patients change, as a result of which the border of death is pushed into the future. From the point of view of scientists - supporters of cryonics and nanomedicine, most 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 spots with localization in sloping places of the body, then there isrigor mortis then cadaveric relaxation, cadaveric decomposition ... Rigor mortis and cadaveric decomposition usually begin in the muscles of the face and upper extremities. The time and duration of these signs depends on the initial background, temperature and humidity of the environment, the reasons for the development of irreversible changes in the body.

The biological death of a subject does not mean a one-stage biological death of tissues and organs that make up his body. The time to death of the tissues that make up the human body is mainly determined by their ability to survive under conditions of hypoxia and anoxia. This ability is different for different tissues and organs. The shortest lifetime under anoxia is observed in the brain tissue, more precisely, in the cerebral cortex and subcortical structures. The stem sections and the spinal cord have greater resistance, or rather resistance to anoxia. Other tissues of the human body have this property to a more pronounced degree. So, the heart retains its viability for 1.5-2 hours after the onset of biological death. The 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 biological death. Bone tissue, being the most inert tissue of the human body, retains its vitality for up to several days. The phenomenon of surviving organs and tissues of the human body is associated with the possibility of their transplantation, and the earlier after the onset of biological death organs are removed for transplantation, the more viable they are, the more likely their further successful functioning in another organism.

2.The clothes are removed from the corpse, placed on a specially designed gurney on the back with the knees extended, the eyelids are closed, the lower jaw is tied, covered with a sheet and taken to the sanitary room of the department for 2 hours (until the appearance of cadaveric spots).

3. Only after that the nurse writes on the deceased's thigh his surname, initials, medical history number and the corpse is taken to the morgue.

4. Things and valuables are transferred to relatives or friends of the deceased on 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 given for disinfection. The bed, the bedside table are wiped with a 5% solution of chloramine B, the bedside vessel is soaked in a 5% solution of chloramine B.

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

7. It is necessary to report the death of the patient to the admission department of the hospital, 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 station.

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

The etiopathogenetic mechanisms of acute respiratory disorders, as well as the manifestation of the syndrome, have many features. Unlike chronic acute respiratory failure, it is a decompensated state in which hypoxemia, hypercapnia rapidly progress, and blood pH decreases. Disturbances in the transport of oxygen and CO2 are accompanied by changes in the functions of cells and organs. Acute respiratory failure is one of the manifestations of a critical condition, in which even with timely and correct treatment, 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 damage to the lungs (pulmonary parenchyma, capillaries and alveoli), accompanied by significant gas exchange disorders. 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 impaired, 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 a “target” organ that responds to any changes in metabolism. Critical mediators pass through the filter, causing damage to the ultrastructure of the lung tissue. Pulmonary dysfunction of one degree or another always occurs with severe influences - 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).

Ventilation respiratory failuremanifested 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:

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

 Violations of 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.

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

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

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

Causes of parenchymal respiratoryinsufficiency:

 Trauma, sepsis, systemic inflammatory reaction (released inflammatory mediators: tumor necrosis factor, pro-inflammatory cytokines, thromboxane, NO, arachidonic acid metabolites, impaired oxygen transport in case of damage to lung functional units by oxygen radicals passing through the pulmonary filter;

 Syndrome of multiple organ failure (in these cases, lung damage usually occurs);

 Respiratory distress syndrome in adults;

 Severe forms of pneumonia;

 Bruised lungs;

 Atelectasis;

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

 Severe form of bronchial asthma;

 Pulmonary embolism;

 Massive bronchopulmonary aspiration.

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

Clinical pictureacute respiratory failure can be erased during an external examination of the patient and even be absent, but it can also have an extremely pronounced character.

Ventilation 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 Рco2 leads to the 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 the volume of ventilation of the lungs, even apnea, may be observed. With the development of ventilation respiratory failure in a patient with an initially clear consciousness, blood pressure rises (often up to 200 mm Hg and above), cerebral 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 the lethargy disappears. Hypercapnia is also characterized by oliguria, which is always observed with pronounced respiratory acidosis.

Decompensation of the state occurs at the moment when the high level of Рco2 in the blood ceases to stimulate the respiratory center. Signs of decompensation in far-reaching 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. In this case, РСО2 reaches 100 mm Hg, but coma may occur earlier - due to hypoxemia. At this stage, it is necessary to carry out artificial ventilation of the lungs with a high FiO2. The development of shock against the background of a coma means the onset of rapid damage to the cellular structures of the brain, internal organisms 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, lack of expression of clinical symptoms and the possibility of death within a short time. First, tachycardia with moderate arterial hypertension develops, nonspecific neurological manifestations are possible: inadequacy of thinking, confusion of consciousness and speech, lethargy, and so on. Cyanosis is a relatively subjective factor observed only in the late stage of acute respiratory failure. And corresponding to a significant decrease in saturation and oxygen tension in arterial blood (SaO2< 80%, Po2 < 50ммHg). Внезапно нарушается сознание и развивается кома (гипоксическая) с отсутствием рефлексов, падением артериального давления, остановкой сердечной деятельности. Продолжительность гипоксемической формы острой дахательной недостаточности может колебаться от нескольких минут (при аспирации, асфиксии, синдроме Мендельсона) до нескольких часов и дней (респираторный дистресс синдром взрослых).

Clinical signs of progressive respiratory failure:

 Respiratory disorders (shortness of breath, gradual decrease in respiratory and minute volumes of respiration, oligopnea, unexpressed cyanosis);

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

 Disorders 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 breathing disorder (oligoproe, tachypnea, bradypnea, apnea, pathological rhythms);

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

 Progressive hypercapnia (Рco2< 50 мм Hg);

 pH< 7,30.

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

Acute heart failureis a sudden onset of muscle failure of the ventricles of the heart. This condition can be exacerbated by a dissonance between a decrease in the work of one and the normal function of another part of the heart. Suddenly developing heart weakness can be fatal.

The causes of acute cardiac abnormalities are myocardial infarction, diffuse myocarditis, excessive physical activity, intercurrent infection, as well as other pathological conditions in which hypercatecholaminemia is observed, a violation of the ionic composition of the intracellular fluid, conduction disturbances, especially in the atrieventricular system (attacks of Morgagni - Edems - Stokes ), impaired excitability (attacks of paroxysmal tachycardia, paroxysmal atrial 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 the blood filling of the arterial system, is very reminiscent of the picture of acute vascular circulatory failure, 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 low pulse filling. Recognition of acute weakness of the heart is based primarily on the detection of changes in the heart (expansion of the boundaries of the heart, arrhythmia, prodiastolic gallop rhythm). At the same time, shortness of breath, swelling of the cervical veins, congestive wheezing, 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 heart weakness than vascular. Blood pressure is reduced. There are symptoms of organ ischemia with symptoms of venous congestion due to a disproportion between the total mass of circulating blood and its effective volume.

Acute syndrome right ventricular failureit is most prominently 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 has shortness of breath, cyanosis, sweat, a feeling of constriction 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 builds up, the cervical veins swell, and then the liver enlarges, the accent of the II tone on the pulmonary artery and the gallop rhythm are heard. Radiographically determined enlargement of 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 pulmonary 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 are admitted to the surgical department with a diagnosis of acute abdomen and acute cholecystitis due to severe pain in the right hypochondrium due to stretching of the liver capsule.

Sharp left ventricular failureclinically manifested by cardiac asthma and pulmonary edema.

Cardiac asthma is an upcoming asthma attack.

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 opening with a movable thrombus in mitral stenosis. Characterized by the disappearance of the arterial pulse, along with a palpable strong heartbeat, the appearance of acute pain in the heart, shortness of breath, increasing cyanosis with subsequent loss of consciousness and the development of reflex collapse in most cases. Prolonged closure of the atrioventricular opening by a thrombus, as a rule, leads to death of patients.

Similarly, with mitral stenosis, a syndrome of acute functional failure of the left atrium is often observed. This happens when the defect is compensated by the increased work of the left atrium with the preserved contractile function of the right ventricle. With excessive physical exertion, a sudden stagnation of blood in the vessels of the lungs can occur and an attack of cardiac asthma can occur, 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 on the vessels of the lung.

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

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

With physical exertion, excitement, fever, pregnancy, etc., there is an increased demand for oxygen in the body, increased cardiac activity and increased minute volume, which in patients with already existing heart lesions can lead to sudden onset of weakness of the left heart. The decompensated difference in the ejection of blood from the right and left heart leads to overflow of the small circle, blood circulation. Pathological reflexes due to hemodynamic disturbances lead to the fact that the production of glucocorticoids decreases, and mineralocorticoids increase. 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 a large role in the development of these complications - this is a violation of lymph circulation in the lung tissue, expansion of the anastomoses between the veins of the large and small circle.

Prolonged increase in capillary pressure in the lungs above 30 mm Hg. Art. causes fluid from the capillaries to leak 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. The thickening and fibrosis of the alveolar wall can prevent the development of pulmonary edema with high capillary pressure. With increased permeability of capillaries (anoxemia, infections, anaphylactic shock, etc.), pulmonary edema can develop even when the capillary pressure is significantly below 30 mm Hg. Art. Pulmonary edema occurs in patients with a small difference between the pressure in the pulmonary artery and pulmonary capillaries and low pulmonary arteriolar resistance. When the pressure gradient between the pulmonary artery and pulmonary capillaries is high, there is a high pulmonary arteriolar resistance, which creates a protective barrier that protects the pulmonary capillaries from overfilling them with blood, a sharp increase in pressure in them, and, consequently, from the occurrence of cardiac asthma or pulmonary edema ... In patients with pronounced narrowing of the left venous 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 partial loss of elasticity of the lung tissue were noted. In this regard, the pulmonary capillaries are removed from the alveolar membrane, the alveolar membranes themselves thicken. This restructuring begins when the pressure in the pulmonary artery increases to 50 mm Hg. Art. and higher and is most pronounced in the pulmonary vessels with an increase in pulmonary arterial pressure 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 attacks of suffocation or pulmonary edema in them. Capillary extravasation is also possible with these changes, but at a higher "critical" level of pulmonary capillary pressure, which is necessary for capillary extravasation and the passage of tissue fluid through altered alveolar membranes.

Clinic for Cardiac Asthma and Pulmonary Edemacharacterized at first by the occurrence of severe suffocation and severe cyanosis. In the lungs, a large number of scattered dry and wet wheezing is determined. Bubbling breathing appears, coughing with frothy sputum (often stained with blood). Blood pressure often decreases.

Acute renal failure (ARF)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 tendency in which acute renal failure is detected as one of the manifestations of multiple organ failure syndrome.

CAUSES

All the reasons that cause the development of ARF can be conditionally divided into three large groups:

1. Extrarenal (extrarenal) causes- lead to a decrease in the BCC and a sharp decrease in renal blood flow, which can cause irreversible death of renal tissue cells. The extrarenal causes of acute renal failure include: severe extensive 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 renal tissue lesions, acute inflammation of the renal parenchyma or renal vascular lesions, which cause renal tissue necrosis. Renal causes of acute renal failure include: acute glomerulonephritis; acute tubular necrosis; rheumatic kidney damage; blood diseases; poisoning with salts of mercury, copper, cadmium, poisonous mushrooms, organic fertilizers; malignant arterial hypertension; lupus nephritis; uncontrolled intake of drugs from the sulfonamide group, antineoplastic 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 calyx-pelvic system, edema and necrosis of renal tissue cells. 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 during trauma, surgical interventions on the abdominal organs.

CLASSIFICATION

Depending on the causes of development, prerenal, renal and postrenal ARF are isolated, respectively.

SYMPTOMS

With acute renal failure, there is a sharp violation of all 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 impaired renal excretory function, one of the main symptoms of acute renal failure develops - oliguria (decreased urine output) up to anuria (complete absence of urine). The condition of patients with acute renal failure is usually moderate or severe, impaired consciousness (lethargy or excessive excitement), edema of the extremities, heart rhythm disturbances, nausea and vomiting, and an increase in the size of the liver.

The clinical course of ARF 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 can be different, it is determined by the main cause of ARF development.

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 complete absence of urination. This stage usually develops within three days from the onset of ARF, but can extend to 5-10 days. Moreover, 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, and may fall into a coma. Due to the pronounced suppression of immunity, the risk of a secondary infection increases with the development of pneumonia, stomatitis, parotitis, etc.

3. During the diuretic stage, a gradual increase in urine volume occurs, 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 the symptoms of renal failure, restoration of the electrolyte balance of the blood.

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

Acute liver failuredevelops 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 ARF is hepatic encephalopathy (HE), which decisively affects the course of ARF and the prognosis of the disease.

ARF can be talked about if encephalopathy develops within 8 weeks from the onset of the first symptoms of acute hepatocellular failure. If PE develops within 8 to 24 weeks from the onset of the first symptoms of liver damage, then we should talk about subacute hepatic 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. Poisoning with drugs (paracetamol).

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

4. Wilson-Konovalov's disease.

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

The main symptoms and complications of ARF

Hepatic Encephalopathy is a complex of potentially reversible neuropsychiatric disorders resulting from acute or chronic liver failure and / or portosystemic blood shunting.

According to most researchers, PE develops due to the penetration of endogenous neurotoxins through the blood-brain barrier (BBB) \u200b\u200band their effect on astroglia as a result of liver cell failure. In addition, the amino acid imbalance that occurs in liver failure affects the development of HE. As a result, the BBB permeability, the activity of ion channels change, neurotransmission and the provision of neurons with high-energy compounds are impaired. 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 blood shunting. Ammonia in 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 into the brain, as a result of which the synthesis of false neurotransmitters and serotonin is enhanced.

According to a number of authors, in addition to ammonia, the 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. Their mechanisms of action are similar and are associated with 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 supply of which to 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 reinforcement of several factors: endogenous neurotoxins, among which ammonia is of leading importance, amino acid imbalance and changes in the functional activity of neurotransmitters and their receptors.

The development of encephalopathy in patients with acute renal failure is dominated by factors of parenchymal liver failure, the outcome of which is often endogenous hepatic coma. In this case, the provoking factors are the increased breakdown of proteins contained in the diet, or when blood protein gets in with gastrointestinal bleeding, irrational intake of drugs, alcoholic 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 standardization of the nomenclature, diagnostic signs and prognosis of liver and biliary tract diseases (C. Leevy et al., 1994), latent and clinically expressed (4 stages) PE ...

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 bilirubin level can increase up to 900 μmol / L.

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

4. Flopping tremor. Determined in conscious patients. In addition, it can be 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 platelet count also decreases. As a consequence, 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) - increased cardiac index, low peripheral resistance, arterial hypotension;

hypovolemia;

enlargement of the heart;

pulmonary edema;

arrhythmias (atrial fibrillation and ventricular extrasystoles);

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

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

10. Renal failure (hepatorenal syndrome). Most patients with acute renal failure have renal failure, which is manifested by oliguria, an increase in blood creatinine levels. In case of acetaminaphen poisoning, 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. Blood urea levels in ARF tend to be low as a result of decreased liver synthesis.

The differential diagnosis of acute (fulminant) liver failure should be carried out with bacterial meningitis, brain abscess, encephalitis.

"

General disabilities in acute surgical diseases of the abdominal organs are mainly due to intoxication.

Endogenous intoxication - (lat. in in, inside + Greek. toxikon poison) - 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 impaired homeostasis due to the accumulation of endogenous toxic substances in the body 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 is 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.

The terms "detoxification" and "detoxification" are used to denote the processes of elimination of endotoxicosis. The latter term is more often used to characterize therapeutic methods for 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, stunnedness, 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 in 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, seizures of soporous or even coma. In infectious diseases, a typically febrile state with signs of intoxication psychosis. The 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, disturbances in the rhythm and conduction of the heart), usually accompanied by respiratory disorders (shortness of breath, cyanosis of the mucous membranes, metabolic acidosis). Hepato- and nephropathy is 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 few laboratory tests have been proposed. One of the first to use integral indicators of 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, in nephropathy, the composition of urine, the concentration of creatinine, urea in plasma, etc., are examined; in 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 indicators (the level of T- and B-lymphocytes, immunoglobulins of class G, A, M, 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 during trauma, enzyme activity - in pancreatitis, bacteremia - in sepsis.

1) etiological, which aims to accelerate the elimination 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, to increase the body's immunological defense;

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

In addition, the entire arsenal of drugs for treating the underlying disease that led to the development of endotoxicosis is simultaneously used. Most often it is antibacterial treatment, specific pharmacotherapy, surgical aid, etc.

For the purpose of detoxification, intravenous infusion therapy (solutions of glucose, electrolytes, hemodesis) 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).

In order to remove toxins from the blood, hemofiltration is used ( hemodialysis )or hemosorption, as well as the operation of plasmapheresis (purification of blood plasma). In case of symptoms of overhydration of the body or a high concentration of toxins in the blood and lymph, it is recommended lymphatic drainage and purification of the received lymph (lymphosorption) with its subsequent return to the body (intravenous drip infusion) in order to avoid possible loss of proteins.

The greatest efficiency of detoxification is achieved with the combined use of several methods and the use of various biological media (blood, lymph) to cleanse.

The pathogenetic treatment of endotoxicosis consists in the use of antiproteolytic drugs (contrikal, trasilol or ingitril), antioxidants (tocopherol), immunostimulants (T-activin).

The greatest effect in this regard is possessed by ultraviolet irradiation of blood 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 CM and other laboratory parameters of endotoxicosis until their stable normalization.

Forecast is largely associated with the possibilities of using modern methods of artificial detoxification in the early stages of the development of endotoxicosis.