PATHOPHYSIOLOGY OF THE EXTREME STATES.

SHOCK. COLLAPSE. COMA PATHOPHYSIOLOGY OF EXTREME STATES. SHOCK. COLLAPSE. COMAProfessor Yu.I. Bondarenko

Extreme states are 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.).

• Preterminal and terminal states 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.

The most important extreme states:

• SHOCK.

• COLLAPSE.

• COMA

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.

• 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 for realization 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.

• 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 all hypoxia, are observed. In some cases hypoxia is initial etiological factor which results in development of extreme condition. However, more often hypoxia appears secondary during development of extreme condition caused by any other influence.

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 coagulation of 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.

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.

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.

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.

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

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.

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).

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

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).

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).

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.

The second (vasodilating) type of compensatory reaction

• Directed on elimination of ischemia.

• Vasoactive amines are formed cause dilation of vessels

• Increase of vessels permeability

• Disorder of reological properties of blood.

• Disintegration of cells, activation of proteolytic enzymes, output from cells potassium ions.

• 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.

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.

Stage 1: Anticipation stage

Stage 2: Pre-Shock Slide

Stage 3: Compensated Shock

Stage 4: Decompensated Shock, reversible

Stage 5: Decompensated Shock, Irreversible

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.

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.

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.

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).

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.

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.

Collapse

Collapse is an acute vascular insufficiency is characterized by fall of a vascular tone and also acute

reduction of circulating blood volume .• Reduction of venous blood inflow to heart.

Decrease of heart output.• Fall of arterial and venous pressure. • Disorder of tissues perfussion and metabolism.

Hypoxia of brain development.• Vital functions of an organism are oppressed.• It is shown in clinic by short-term of consciousness

loss.

Classification. Etiology, pathogenesis and consequences.

• The infectious collapse develops as complication of acute infectious diseases: meningoencephalitis, and typhoid fever typhus fever, acute dysentery, pneumonia, botulism, the Siberian ulcer, virus hepatites, toxic influenza. The reason of such complication is the intoxication by endo- and exotoxins of microorganisms, mainly that influence on central nervous system, or receptors of pre- and postcapillaries.

• Hypoxic collapse may appear in conditions of reduced partial pressure of oxygen in air. The direct reason is insufficiency of adaptive reactions of an organism to hypoxia. To development of collapse may promote also hypocapnia owing to hyperventilation

Ortostatic collapse

• Appears at fast transition from horizontal position to vertical

• At long time of standing.

• At redistribution of blood with increase of total amount of a venous system

• At decrease of inflow to heart.

• In basis of this condition is insufficiency of a venous tone lays.

Ortostatic collapse • Observed at recovers after heard diseases of endocrine

and nervous system• In the postoperative period• At fast removal of ascitic liquids • As a result of spinal and peridural anesthesias. • Ortostatic collapse may be observed at recovers after

heard diseases of endocrine and nervous system • Iatrogenic ortostatic collapse sometimes appears during

wrong use of neuroleptics, ganglioblockers, adrenoblockers, sympatolytics.

• Among pilots and cosmonauts ortostatic collapse may be caused by redistribution of blood.

• It may be observed at practically healthy children and teenagers.

Hemorrhagic collapse

• Develops at massive blood loss as a result of fast reduction of circulating blood.

Collapse also may be observed:

• At acute diseases of internal organs ( peritonitis, acute pancreatitis, duodenitis, erosive gastritis)

• At diseases of heart which are accompanied by acute and fast reduction of stroke volume (heart infarction, disorders of heart rhythm, acute myocarditis or pericarditis with accumulation of exudate in pericardium).

Pathogenesis: 1. Fall of venous and arterioles tone as a result of action of

infectious, toxic, physical, allergic and other factors directly on a vascular wall, vasomotoric centre and vascular receptors (sinocarotid zones,arches of an aorta).

2. Fast reduction of circulating blood volume (blood loss,plasma loss).

3. Reduction of circulating blood volume results in decrease of blood return to heart and heart output.

4. The blood accumulates in capillaries, develops circulatory hypoxia, metabolic acidosis, permeability of vessels increases.

5. It promotes transition of water and electrolytes from blood in intercellular space, are damaged reologic properties of blood, there is a hypercoagulation of blood and pathological aggregation of erythrocytes and thrombocytes that creates conditions for formation of microblood clots.

Cоmа

• Cоmа is a pathological state that is characterized with deep oppression of functions of the central nervous system and it is shown by loss of consciousness, absence of reflexes on external irritators and disorders of the vital functions regulation of an organism.

Classification. Etiology. Pathogenesis.

• 1. Cоmas at initial injury and diseases of the central nervous system (insult, craniocerebral trauma).

• 2. Cоmas in the endocrine diseases that apper as at insufficiency of some glands of internal secretion (diabetic, hypocorticoid, hypopituitary, hypothyreoid), and at their hyperfunction (thyreotoxic, hypoglycemic).

• 3. Toxic cоmas are observed at endogenic ( uraemia, hepatic insufficiency, toxicoinfections, pancreatitis) and exogenic intoxications (alcoholic poisonings, barbiturate poisoning, phosphororganic poisoning.

• 4. Cоmas caused by infringements of gas exchange at various kinds of hypoxias.

• 5. Cоmas caused by loss of electrolytes, water and energetic substances.

Cоmа is stage of development of some diseases. In their pathogenesis is lesion of the central nervous system with disorder of function of cortex brain, subcortex formations and trunk brain that results in loss of consciousness.

The main pathogenetic mechanisms

• 1. Disorder of cellular breath and an exchange of energy in brain. A basis of them is hypoxia, anemia, disorders of brain blood circulation, blockade of respiratory enzymes by cytotoxic poisons, acidosis (at diabetic and uraemic cоma), deficiency of power substances or blockade of their recycling (starvation, hypoglycemis coma). In development of brain hypoxia disorders of microcirculation play role. Owing to hypoxia it is broken oxidizing phosphorelation, the content and use АТP and creatinphosphate decreases.

• 2. Disorder of synaptic transmission in the central nervous system. It may be connected with:

• a) disorder of synthesis, transport, deposition and secretion of neuromediators;

• b) replacement of neuromediators by pseudomediators;

• c) excessive activation of inhibition postsynaptic receptors;

• d) blockade stimulating postsynaptic receptors. This mechanism has the great value in development of hepatic, uremic and toxic comas.

• 3. Disorder of electrolyte balance with changes of cellular potentials and process of polarization of neurons membranes, and also infringement of osmotic pressure.

• 4. Changes of physical properties and structures of brain and intracranial formations. Pathogenetic value has swelling and edema of brain and brain membrane, increase of intracranial pressure which strengthen infringement of hemodynamics and liquordynamic, make hypoxia of nervous cells heavier and oppress their physiological activity. Mechanical damage of brain matters cells at a craniocerebral trauma, tumours, hemorrhage in brain.