pathophysiology of the extreme states shock collapse coma n.
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PATHOPHYSIOLOGY OF THE EXTREME STATES. SHOCK. COLLAPSE. COMA
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  1. PATHOPHYSIOLOGY OF THE EXTREME STATES. SHOCK. COLLAPSE. COMA PATHOPHYSIOLOGY OF EXTREME STATES. SHOCK. COLLAPSE. COMA Professor Yu.I. Bondarenko

  2. Extreme statesare the conditions of an organism characterized by an excessive straining or an exhaustion of adaptive mechanisms. • 1. Primary - action on an organism of various extreme irritators (for example, traumas, endogenic intoxications, severe fluctuations of air temperature and concentration of oxygen) • 2.Secondary - as a result of adverse course of disease (for example, insufficiency of blood circulation, respiratory, renal or hepatic insufficiency, anemia etc.).

  3. Preterminal and terminalstates may occur when pathogenity of extreme irritator exceeds maximum possibilities of adaptation of an organism, heavy disorders of the vital functions and direct threat of life appear. • Many forms of extreme conditions are convertible, while terminal conditions without special emergency help lead to death of an organism. • In these cases life of the patient depends directly on condition of breath and blood circulation, and also from time which has passed after their stop.

  4. The most important extreme states: • SHOCK. • COLLAPSE. • COMA

  5. Pathogenesis • 1. Activation of sympathoadrenal and pituitary-adrenal systems typical for stress. • 2. In the process of deepening of condition heaviness are realized narrowing of adaptive reactions, disintegration of functional systems which provide complex adaptive behavioural acts and delicate regulation of locomotor and vegetative functions.

  6. One of mechanisms of organism transition in extreme forms of adaptation is progressing unfunctioning of central neurons from various afferentation which provide formation of complex functional systems. • The minimum afferent signals necessary forrealization of breath, blood circulation and other vital functions are reminded only. • Regulation of vital processes basic passes to a metabolic level. In this stage there are expressed disorders of all physiological functions.

  7. Pathogenic chain is characterized for development of extreme conditions that aggravate organism disturbance. • At all extreme conditions similar disturbances of metabolism and physiological functions, first of allhypoxia, are observed. In some cases hypoxia is initial etiological factorwhich results in development of extreme condition. However, more often hypoxia appears secondaryduring development of extreme condition caused by any other influence.

  8. Microcirculatory disorder: • Decrease of perfusion of microvessels • Dilatation and decrease of their sensitivity to vasopresor influences • Increase of permeability of vascular walls and their structural disorders even to necrobiosis • Pathological aggregation of erythrocytes,‘sludg-syndrome’, hypercoagulation of blood, disseminated intravascular coagulationof blood and microthrombosis of vessels • Disturbance of microcirculation in lungs (so-called ‘shock lung’)may result in their severe disorders of gas change functions, similar changes in kidneys (‘shock kidney’)may lead to renal insufficiency.

  9. Hemodynamic system disorder: 1. Decrease of circulating blood volume and speed of blood flow. 2. Increase of blood pooling and decrease of venous return of blood to heart. 3. Fall of arterioles tone and veins even to their paresis. 4. Decrease of general peripheral resistance of vascular system. 5. Tachycardia, various forms of arrhythmias, insufficiency of coronary circulation. 6. Decrease of cardiac output.

  10. Disorders of external breath: • Changes of depth and frequency, rhythm of respiratory movements. • Periodic breath. Disorders of functions of nervous system: • Consciousness lost only at the end of terminal condition.

  11. Shock • Shock is heavy pathological process accompanied with an exhaustion of the vital functions of an organism and results it on border of life and death because of critical decrease of capillary blood circulation in injured organs.

  12. Etiological classification 1. Traumatic; 2. Hemorrhagic; 3. Burn; 4. Tourniquet (develops after removal of jute after four hours and more after imposing); 5. Anhydremic (dehydrative); 6. Cardiogenic; 7. Pancreatic; 8. Septic; 9. Infection-toxic; 10. Anaphylactic

  13. Pathogenic classification 1. Hypovolemic shock (hemorrhagic, anhydremic) 2. Shock connected with disturbances of pump function of heart (cardiogenic) 3. Vascular forms of shock (anaphylactic, pancreatic) 4. Painful shock at which the central regulation of blood circulation (traumatic, after burning) is damaged.

  14. Mechanisms of general hemodynamic and microcirculation disorder in shock 1. Reduction of arterial pressure; 2. Reduction of circulating blood volume ; 3. Decrease of volume speed of organ circulation; 4. Disorder of reologic properties of blood (aggregation of form elements, increase of blood viscosity).

  15. Mechanisms of blood circulation disorders Reduction of volume of circulating blood: 1. Blood loss (hemorrhagic shock) 2. Loss of blood plasma at massive exudative inflammation (burn shock) 3. Liquid flow out of blood vessels into the tissue (anaphylactic shock) 4. Dehydration (anhydremic shock) 5. Redistribution of blood in vascular system

  16. II. Reduction of heart output: 1. Disorder of contractive functions of heart (heart attack of myocardium); 2. Tamponade of heart (heart break, exudative pericarditis); 3. Arrhythmias (fibrillation of ventricles). III. Reduction of the general peripheral resistance: 1. Fall of neurogenic tone of arterioles 2. Reduction of basal tone of vessels under action of biologicaly active substances (anaphylactic, pancreatic shock) or toxic products (traumatic, turnicate, infection-toxic shock).

  17. IV. Disorders of reological properties of blood: 1. Syndrome of intravascular disseminated coagulation of blood (pancreatic shock) 2. Aggregation of form elements of blood (septic, infectious-toxic shock) 3. Hemoconcentration (anhydremic shock).

  18. Compensatory reactions The first (vasocontrictive) type • Absolute hypovolemia results in decrease of arterial blood pressure and decrease of baroreceptors activity. • As a result of activation sympathoadrenal and pituitary-adrenal systems is secreted adrenaline and corticosteroids. • Catecholamines cause consrtiction of vessels through -adrenoreceptors of skin, kidneys. • Takes place centralization of blood circulation, that is maintenance of blood circulation in vital organs and pressure in large arterial vessels.

  19. The second (vasodilating)type of compensatory reaction • Directed on elimination of ischemia. • Vasoactive amines are formed cause dilation of vessels • Increase ofvesselspermeability • Disorder of reological properties of blood. • Disintegration of cells, activation of proteolytic enzymes, output from cells potassium ions.

  20. Inadequate dilatation of vessels • Change of capillary microcirculation in tissues capillary • Strengthening of shunt blood flow • Change of reaction of precapillary sphincters on epinephrines • Increase of permeability of capillary vessels. • Reduction of cardiac output and decrease of arterial pressure. • There are disorders of lungs’ function (shock lung), kidneys, coagulation of blood.

  21. Development of shock depends also on condition of an organism. All factors causing its weakening, promote development of shock. Heavyness of consequences of shock depends first all on infringement of blood circulation of: • a) brain, • b) coronary vessels, • c) kidneys. As a result of these disorders the central regulation of vital functions is damaged, even to development of coma, acute cardiovascular and renal insufficiency. Occurrence of hypoxia, acidosis and intoxication leads to generalized and irreversible damage of cells.

  22. Stage 1:Anticipation stage

  23. Stage 2: Pre-Shock Slide

  24. Stage 3: Compensated Shock

  25. Stage 4: Decompensated Shock, reversible

  26. Stage 5: Decompensated Shock, Irreversible

  27. Traumatic shock develops owing to large damages of tissues. In its clinic two stages are distinguished: • 1) excitation (erectile); • 2) inhibition (torpid). • The stage of excitation is short-term, is characterized by excitation of the central nervous system owing to reception of pain impulses from the injured tissues. • Painful stress lead to strengthening of functions of blood circulation system , breath, endocrine glands (adenohypophysis, medula and cortex of adrenal glands, neurosecretory nucleus of hypothalamus) with liberation in blood of excess quantity corticotropin, adrenaline, noradrenaline, vasopressin.

  28. The stage of inhibition • It is more long (from several hours to about day) • It is characterized with development of inhibition processes in the central nervous system. • General inhibition seizes also the centres of the vital functions (blood circulation, breath), its are broken, owing to hypoxia development. • Hypoxia aggravates disorder in cardiovascular and respiratory centres. • Disorders of hemodynamic and external breath progress vice circle becomes isolated.

  29. Hemorrhagic shock • External bleeding (knife, bullet wound, erosion bleedings of stomach at stomach ulcer, tumors, from lung at tuberculosis etc.) • Internal bleeding (hemothorax, hemoperitonium) bleedings in conditions of tissues traumation. Unhydremic shock • Loss of liquid and electrolytes: 1. During the exudative pleurities, intestinal obturation, peritonitis liquid comes from vascular system into cavities. 2. During the unrestrained vomitting and strong diarrhea the liquid is lost outside. Develops hypovolemia which plays a role of main pathogenetic link.

  30. Burn shock • Appears at extensive and deep burns. • Main pathogenetic factors are hypovolemia, pain irritation, expressed increase of vessels permeability . Septic (endotoxin) shock • Appears as complication of sepsis. • Main damaging (injuring) factor are endotoxins of microorganisms. 1. Increase of requirement of an organism in oxygen owing to amplification of exchange processes, tachypnoe, tachycardia, fever; 2. Decrease of blood oxygenation in lungs and insufficient extraction of oxygen from blood by tissues; 3. Activation by endotoxins of proteolytic systems in biological liquids (kallikrein-kinin, complement, fibrinolytic).

  31. Cardiogenic shock is observed: • 1. Decrease of pump function of cardiac muscle (heart infarction, myocarditis), at heard disorders of heart rhythm (paroxysmal tachycardia) • 2. Tamponade heart (thrombosis of cavities, exudation or bleeding in pericardium) • 3.Massive embolia of lungs arteries (thromboembolia of lungs). Main mechanism cardiogenic shock is reduction of stroke and minute volume of blood, arterial pressure and increase of heart filling pressure.

  32. Anaphylactic shock • Develops owing to liberation of histamine and others vasoactive substances (kinins, serotonin). • Thus there is strong reduction of venous return to heart. The reason of it is dilatation of capillary and capacitor vessels. • The congestion of blood in capillary vessels and veins results in reduction of circulating blood volume. • Disorder of contractive activity of heart is observed also. Sympathoadrenergic reaction thus is not expressed because of a vascular tone disfunction.