EXTREME STATES

PATHOPHYSIOLOGY OF THE nEXTREME STATES.

SHOCK. COLLAPSE. COMA

Definitioof concept. General characteristic. Reasons and mechanisms of development

Extreme states nare the conditions of organism described by an excessive straining or aexhaustion of adaptive mechanisms. Extreme conditions may develop primarily by naction on an organism of various extreme irritators (for example, traumas, nendogenic intoxications, severe fluctuations of air temperature and concentratioof oxygen) or to become a result of adverse course of disease (for example, ninsufficiency of blood circulation, respiratory, renal or hepatic ninsufficiency, anemia etc.).

Whepathogenicity of extreme irritator exceeds maximum possibilities of adaptatioof an organism, heavy disorders of the vital functions and direct threat of nlife appear. In such cases preterminal and terminal conditions may occur. Many nforms of extreme conditions are convertible, while terminal conditions without nspecial emergency help lead to death of  nan organism. In these cases life of the patient depends directly ocondition of breath and blood circulation, and also from time which has passed nafter their stop. The most important and frequently noccuring extreme conditions are collapse, shock and coma.

 Stages of organism vital activity ndisorder in action of  pathogenic  factor

 

Idevelopment of extreme conditions important meaning belongs to activation of nsympathoadrenal and pituitary-adrenal systems typical for stress. In the nprocess of deepening of condition heaviness there are narrowing of adaptive nreactions, disintegration of functional systems which provide complex adaptive nbehavioural acts and delicate regulation of locomotor and vegetative functions. nOne of mechanisms of organism transition on extreme forms of adaptation is nprogressing switching-off of  ncentral neurons from various afferentation which provide formation of ncomplex functional systems. The minimum afferent signals necessary for nrealization of breath, blood circulation and other vital functions are reminded nonly. Regulation of life processes basicly passes to a metabolic level. In this nstage, as a rule, there are expressed infringements of all physiological nfunctions. For pathogenesis of extreme nconditions development of chain of pathological reactions which aggravate norganism disturbance is characteristic.

 

Disorders in  extreme states of insuficiency mechanism nof  adaptation

 

At all nextreme conditions similar disturbances of metabolism and physiological nfunctions, first of all hypoxia, are observed. In some cases hypoxia is initial nethiologic factor which results in development of extreme condition. However, nmore often hypoxia appears secondary during development of extreme conditiocaused by any other influence.

Extreme nconditions are usually accompanied by the strengthened liberation and formatioof histamine, serotonin, kinins, lysosomal enzymes and other biologically nactive substances. Therefore to extreme conditions disturbances of nmicrocirculation are peculiar: infringement of perfusion of microvessels, ndilatation and decrease of their sensitivity to vasopressing influences, nincrease of permeability of vascular walls and their structural infringements neven to necrobiosis. Pathological aggregation of erythrocytes, ‘sludg-syndrome’, nhypercoagulation of blood, disseminated intravascular coagulation of blood and nmicrothrombosis of vessels. Disturbance of microcirculation in lungs (so-called n‘shock lung’) may result in their severe infringements of gas nchange functions, similar changes in kidneys (‘shock kidney’) may nlead to renal insufficiency. Infringements of microcirculation system in liver nand brain may cause hepatic insufficiency and severe disturbances of nervous nsystem.

At all nextreme conditions infringements of hemodynamic system is observed, described nby decrease of volume of circulating blood and speed of blood flow, increase of nblood deposition, decrease of venous return of blood to heart, fall of tone of narterioles and veins even to their paresis and decrease of general peripheral nresistance of vascular system are observed also. As to the heart, the ntachycardia, various forms of arrhythmias, insufficiency of coronary ncirculation, decrease of cardiac output and other attributes, characteristic nfor heart insufficiency are frequently observed.

Infringements nof external breath during the extreme conditions are shown by various changes nof its depth and frequency, rhythm of respiratory movements, periodic breath.

Infringements nof functions of nervous system at early stages of development of an extreme ncondition are various. So, at the majority kinds of shock after the period of nthe general excitation in erectile phase original combination of the kept nconsciousness with the general deep block in torpid phase is typical. nConsciousness is lost only at the end of this phase at transition to a terminal ncondition.

Shock. Classification. Ethiology, pathogenesis, consequences

Shock is grave npathological process accompanying with an exhaustion of the vital functions of nan organism and resulting it on a side of life and death because of critical ndecrease of capillary blood circulation in lesion organs.

 

The basic kinds of shock

Depending non the reasons of occurrence there are following kinds of shock:         n1) traumatic;

2) nhemorrhagic;

3) burn;

4) nturnicate (develops after removal of jute after four hours and more after nimposing);

5) anhydremic n(dehydrative);                    n

6) cardiogenic;

7) pancreatic;

8) septic;

9) ninfectional-toxic;

10) anaphylactic.  

Depending othe initial mechanisms underlying in pathogenesis of shock there are:

1) nhypovolemic shock (hemorrhagic, anhydremic);

2) nshock connected with disturbances of pump function of heart (cardiogenic);   3) vascular nforms of shock (anaphylactic, pancreatic);

4) npain shock at which the central regulation of blood circulation (traumatic, nafter burning) is damaged.

 

Mechanisms of general nhemodynamics infringements  and nmicrocirculation during shock

Irrespective nof the reasons of occurrence the shock is shown by a complex of infringements nof hemodynamics for which are characteristic:

1) nreduction of arterial pressure;

2) reductioof circulating blood volume ;

3) decrease nof volumetric speed of organ circulation;

4) infringement of reologic properties of nblood (aggregation of form elements, increase of blood viscosity).

 

The ncomplex of the specified infringements is designated as acute insufficiency of nblood circulation. Initial infringement of its parameters at any version of nshock leads again to infringements of all others.

Ibasis of development of blood circulation disorders  at shock the following mechanisms may nlay.

I. nReduction of volume of circulating blood:

1)    nblood loss (hemorrhagic shock);

2)    nloss of blood plasma at massive nexudative inflammation (burn shock);

3)    nan exit of fluid from blood vessels n(anaphylactic shock);

4)    ndehydration (anhydremic shock);

5)    nredistribution of blood in vascular nsystem (thrombosis and embolism of main veins).

 

II. nReduction of minute volume of heart:

1) infringement of contractive functions of heart n(heart attack of    myocardium); n

2) ntamponade of heart (heart break, exudative pericarditis);

3) narrhythmias (fibrillation of ventricles).

 

III. nReduction of the general peripheral resistance in result of generalized ndilation of vessels:

1)    nfall of neurogenic tone of arterioles n(pain forms of shock);         n

2) nreduction of basal tone of vessels under action of biologicaly active nsubstances (anaphylactic, pancreatic shock) or toxic products (traumatic, nturnicate, infection-toxic shock).

IV. nInfringements of reologic properties of blood:

1) syndrome of intravascular disseminated coagulatioof blood (pancreatic shock);

2) naggregation of form elements of blood (septic, infection-toxic shock);

3) nconcentration of blood – hemoconcentration (anhydremic shock). nCorrelation and expressiveness of pathogenetic mechanisms of each kind of shock nare various. At the same time in mechanisms of development of all kinds of nshock it is possible to allocate the common part. It is submitted by nconsecutive inclusion of two types of compensatory-adaptive mechanisms.

 

The nfirst (vasocontractive) type – activation of sympathoadrenal and npituitary-adrenal systems. They are activated by main pathogenetic parts. nAbsolute hypovolemia (loss of blood) or relative (decrease of minute volume of nblood and venous return to heart) results in decrease of arterial pressure of nblood and decrease of baroreceptors  nactivity , which through the central nervous system activates some nadaptive mechanism. The pain irritation, sepsis stimulate its switching. As a nresult of activation sympathoadrenal and pituitary-adrenal systems there is aemission adrenaline and corticosteroids. Epinephrines would cause nconsrtiction  of vessels through a-adrenoreceptors nof skin, kidneys, organs of abdominal cavity). Circulation in these organs is nsharply limited. Coronary and brain vessels do not have  a-adrenoreceptors nand do not constrict. Centralization of blood circulation, that is presented by nremaining of blood circulation in vital organs and pressure in large arterial nvessels takes place.

However, nacute restriction of blood circulation in skin, kidneys, organs of abdominal ncavity causes their ischemia. Hypoxia appears. It switches the second n(vasodilating) type of the mechanisms directed on elimination of ischemia. nVasoactive amines are formed, causing dilation of vessels, increase of their npermeability and infringement of reologic properties of blood. Besides there is na disintegration of corpulent cells, activation of proteolytic enzymes, output nfrom cells potassium ions. There is an inadequate dilatation of vessels, change nof microcirculation in tissues, decrease of capillary and strengthening of nshunt blood flow, change of reaction of precapillary sphincters on epinephrines nand increase of permeability of capillary vessels. Thus, the fluid goes out nfrom the vessels into tissues and venous return decreases. Vice circle appears nat level of cardiovascular system, leading to reduction of cardiac output and ndecrease of arterial pressure. There are disorders of lungs’ functio(shock lung), kidneys, coagulation of blood. Development of shock depends also ocondition of an organism. All factors causing its weakening, promote ndevelopment of shock.

Heaviness nof consequences of shock depends first all on infringement of blood circulatioof:

a) nbrain,

b) ncoronary vessels,

c) nkidneys.

As na result of these disorders the central regulation of vital functions is ndamaged, even to development of coma, acute cardiovascular and renal ninsufficiency. Occurrence of hypoxia, acidosis and intoxication leads to ngeneralized and irreversible damage of cells.

 Each kind of  shock has its features of development.

 

Traumatic shock ndevelops owing to large damages of tissues. In its clinic two stages are ndistinguished:

1) nexcitation (erectile);

2) ninhibition (torpid).

The nstage of excitation is short-term, is characterized by excitation of the ncentral nervous system owing to reception of pain impulses from the injured ntissues.

Thus, npain stress which is shown by strengthening of functions of blood ncirculation  system , breath, some nendocrine glands (adenohypophysis, brain and cortex substances of adrenal nglands, neurosecretory nucleus of hypothalamus) with liberation in blood of nsuperfluous quantity of corticotropin, adrenaline, noradrenaline, vasopressidevelops.

 

The nstage of inhibition is more  long (from nseveral hours to about day) and is characterized by development inhibitioprocesses in the central nervous system.

General ninhibition seizes also the centres of the vital functions (blood circulation, nbreath), they are broken, owing to what oxygen starvation develops. Hypoxia, iturn, aggravates infringements in cardiovascular and respiratory centres. nDisorders  of haemodynamic and nexternal breath progress vice circle becomes isolated.

Except nervous – nreflex mechanisms in occurrence and development of  traumatic shock the certain role plays nalso toxaemia, caused by absorbcion in blood of products of impractical tissues ndisintegration. Recently special value is  ngiven to so-called ischemic toxin. Participation of toxic products ipathogenesis  traumatic shock is nproved by experiments with crossed  nblood circulation.

 

General display of shock n(stage decompensation)

 

 

  Hemorrhagic nshock appears during external (knife, bullet wound, erosiobleedings of  stomach at  stomach ulcer, tumors, from lung at  tuberculosis etc.) or internal n(hemothorax, hemoperitonium) bleedings in conditions of tissues   traumation.

Anhydremic shock appears nowing to significant dehydratation at  nloss of  liquid and nelectrolytes. During the exudative pleurities, intestinal obturation, nperitonitis liquid comes from  nvascular system into   ncavities. During the unrestrained vomitting and strong diarrhea the nliquid is lost outside. Develops hypovolemia which plays a role of maipathogenetic link.

Burn shock nappears at extensive and deep burns. Thus in the first day permeability of ncapillaries is sharply increased, especially in  zone of  burn that leads to  significant exit of  liquid from vessels into tissues. A nlarge amount of edematic liquid, mainly in  nplace of damage, evaporates. Main pathogenetic factors are hypovolemia, npain irritation, expressed increase  nof vessels permeability .

Septic (endotoxin) shock nappears as complication of sepsis. Main ndamaging (injuring) factor are endotoxins of microorganisms. The most oftereason of  sepsis are grammnegative nmicroorganisms, and also streptococci, staphylococci, pneumococci and many nothers.

Maipathogenetic parts of  septic shock:

1) nIncrease of requirement of an organism in oxygen owing to amplification of nexchange processes, tachypnoe,  ntachycardia,  fever. Thedecrease of the general peripheral resistance of vessels is observed;

2) nDecrease of  blood oxygenation ilungs and insufficient extraction of oxygen from blood by tissues. nOxygenation  is decreased iconnection due to circulation infringements in a small circle, aggregation of ntrombocytes on walls of vessels;

   3) Activation by nendotoxins of proteolytic systems in biological liquids n(kallikrein-kinin’s, complement, fibrinolytic).

Cardiogenic  shock is observed nat decrease of pump function of  ncardiac muscle (heart infarction, myocarditis), at heard disorders nof  heart rhythm (paroxysmal tachycardia), nat tamponade heart (thrombosis of cavities, exudation or  bleeding in pericardium), at massive nembolia of lungs arteries (tromboembolia of lungs). Main mechanism cardiogenic na shock is reduction of stroke and minute volume of blood, arterial pressure nand increase of heart filling pressure. As well as at anhydremic  shock, owing to sympathoadrenergic nreactions, the tachycardia, increase of peripheral resistance of vessels is nobserved.

Anaphylactic shock ndevelops owing to increased sensitivity of an organism  to substances of an antigenic nature and naccumulation histamine and others vasoactive substances (kinins, serotonin). nThus there is strong reduction of venous return to heart. The reason of it is ndilatation of capillary and capacitor vessels. The congestion of blood icapillary vessels and veins results in reduction of circulating blood  volume. Infringement of contractive nactivity of heart is observed also. Sympathoadrenergic reaction thus is not nexpressed because of a vascular tone  ninfringement.

Collapse.  Classification. Ethiology, pathogenesis nand consequences.

Collapse is an acute vascular insufficiency  which is characterized by fall of a nvascular tone, and also acute reduction of circulating blood  volume .

At nthe collapse there is a reduction of venous blood  inflow to heart, decrease of heart noutput, fall of arterial and venous pressure, infringement of tissues nperfussion and  metabolism, comes nhypoxia of brain appears, the vital functions of an organism are noppressed. 

 

Exampls:

             n– postinfarction                   – posthemorrhagic             –  hyperthermal

             n– arythmic                   n        –  dehydrotative         n        – ortostatic   n

             n– cardiomyopathic               – toxic–infectious              – toxic

                                                         n– ortostatic                 n       –  anaphilactic          n      

 

It nis shown in clinics by short-term loss of consciousness, general weakness, nfeatures of acute vascular insufficiency with infringements hemodynamics npractically in all organs and tissues.

Ia basis of development of collapse discrepancy between volume of circulating nblood and capacity of a vascular system lays. The reasons may be suddereduction of blood volume (blood loss, dehydratation), and sudden dilatation of nvessels. Collapse develops as complication at heard diseases and pathological nconditions.

The infectious collapse ndevelops as complication of acute infectious diseases: meningoencephalitis, and ntyphoid fever typhus fever, acute dysentery, pneumonia, botulism, the Siberiaulcer, virus hepatites, toxic influenza. The reason of such complication is the nintoxication by endo- and exotoxins of microorganisms, mainly that influence ocentral nervous system, or receptors of pre- and postcapillaries.

 Hypoxic collapse may appear in conditions of reduced partial npressure of oxygen in air. The direct reason of circulation infringements thus nis insufficiency of adaptive reactions of an organism to hypoxia. To ndevelopment of collapse in these conditions may promote also hypocapnia owing nto hyperventilation which leads to expansion of capillaries and vessels, and nfrom here to deposition and decrease   nof circulating blood volume.

Ortostatic  collapse appears nat fast transition from horizontal position in vertical, and also at long time nof standing. Thus there is a redistribution of blood with increase of total namount of a venous system and decrease of inflow to heart. In a basis of this ncondition insufficiency of a venous tone lays. Ortostatic collapse may be nobserved at recovers after heard diseases of endocrine and nervous system, ithe postoperative period, at fast removal of ascitic liquids or as a result of nspinal and peridural anesthesias. Iatrogenic ortostatic collapse sometimes nappears during wrong use of neuroleptics, ganglioblockers, adrenoblockers, nsympatolytics. Among pilots and cosmonauts ortostatic collapse may be caused by nredistribution of blood at action of acceleration when blood from vessels of nthe upper half of body and a head moves into vessels of organs of abdominal ncavity and inferior extremitus, causing hypoxia of brain. Also it may be observed nat practically healthy children and teenagers.

 

Hemorrhagic collapse develops nat massive blood loss as a result of fast reduction of circulating blood.

Collapse also may be observed at acute diseases of internal organs n(peritonitis, acute pancreatitis, duodenitis, erosive gastritis), at diseases nof heart which are accompanied by acute and fast reduction of strike volume n(heart infarction, infringements of heart rhythm, acute myocarditis or npericarditis with accumulation of exudation in cavity of pericardium).

It nis possible to mark two basic mechanisms in pathogenesis:

 1) fall of  veinis and arteriols tone  as a result of action of infectious, ntoxic, physical, allergic and other factors directly on a vascular wall, nvasomotoric  centre and on vascular nreceptors (sinocarotid zones, arches of an aorta);

 2) fast reduction of circulating blood nvolume (blood loss,plasma loss). Reduction of circulating blood volume results nin decrease of return of blood to heart by veins of the big circle of blood circulatioand heart output.

Thus nthe system of microcirculation is damaged, blood accumulates in capillaries, nthe blood pressure falls, develops circulatory hypoxia, metabolic acidosis, npermeability of vessels increases. It promotes transition of water and nelctrolytes from blood in intercellular space, are damaged reologic properties nof blood, there is a hypercoagulation of blood and pathological aggregation of nerythrocytes and trombocytes, that creates conditions for formation of microblood nclots. At a long lasting collapse as a result of hypoxia and disturbances of nmetabolism are released vasoactive substances (histamine, kinins, nprostaglandins) and formed tissue metabolites – lactic acid,adenosine and its nderivatives which cause  hypotonia.

 

Basic chains of  pathogenesis and general displays of collaps

 

 

 

Progressing nchanges lead to infringement of functions of a brain, deepening of regulatory nand hemodynamic disorders. The death at a collapse comes owing to an exhaustioof power resources of brain, intoxication and disturbances of metabolism.

 

Cоmа. nClassification. Ethiology, pathogenesis, consequences

Cоmа nis a pathological condition which is characterized by deep oppression of nfunctions of the central nervous system and it is shown by loss of nconsciousness, absence of reflexes on external irritators and disorders of the nvital functions regulation of an organism.

By norigin distinguish:

1. nCоmas nat initial injury and diseases of the central nervous system (insult, ncraniocerebral trauma).

2. Cоmas nduring the endocrine diseases which apper as at insufficiency of some glands of ninternal secretion (diabetic, hypocorticoid, hypopituitary, hypothyreoid), and nat their hyperfunction (thyreotoxic, hypoglycemic).

3. Toxic cоmas nare observed at endogenic (uraemia, hepatic insufficiency, toxicoinfections, npancreatitis) and exogenic intoxications (alcoholic poisonings, barbiturate npoisoning, phosphororganic poisoning and by other substances).

4.Cоmas, ncaused by infringements of gas exchange at various kinds  of hypoxias.

5.     nCоmas, caused nby loss of electrolytes, water and energetic substances.

 

Exogenous  factors– pathogenic аgents of environment, as rule , extraordinary forces, toxicity or break down of characteristic.

 

Examples:

–         nVariaty traumatic (as rule, brain) factors (electrical charge, mechanical trauma of head.

      –   Thermal actio(overheat, novercooling, sun stroke).

–         nConsiderable fluctation of barometric pressure (hypo– and hyperbaria).

–         nNeurotropic toxins (аlcohol and its supstitutes, ethylene glycol).

–         nInfectious agents (neurotropic viruses, toxins of   nbotulinus and tetanus, agents malaria, typhus fever, cholera).

–         nExogenous hypoxia and аnоxia.

–         nIonizing radiation (large dose of radiation).

 

Endogenous factors – leading to coma ndevelopment, nare resultate of hard disorders of vital activaty of organism. They are observed nat unfavourable course variaties illnes.

 

Examples:

–         nPathological processe in brain (ischemia, insult, tumor, аbsces, edema).

–         nInsuficiency of circulation blood (hypoxia nof brain).

–         nRespiratory insuficiency (asthmatic states, аsphyxia, edema lung).

–         nPatology of blood system (hemolysis of nerythrocytes, hard anemia).

–         nEndocrinopathies (hypoinsulinism, hypo– and hyperthyrosis, superrenal insuficiency).

–         nLiver insuficiency, disorder of digestiv system (syndrome of nmalabsorbtion, intestinal autointoxication).

–         nRenal insuficiency

–         nComatous state develops at hard progressive course of collaps and shock.

Cоmа nis a stage of development of some diseases. Conducting in their pathogenesis is ndefeat of the central nervous system with infringement of function of cortex nbrain, subcortex formations and trunk brain that results in loss of nconsciousness. A special role in development of coma plays infringement of reticular nformations function with loss of its activating influences on  cortex brain and oppression  of subcortex formations function and  centres of vegetative nervous system. nMain pathogenetic parts in development of coma are:

1. nInfringement of cellular breath and an exchange of energy in brain. A basis of nthem is hypoxia, anemia, disorders of brain blood circulation, blockade of nrespiratory enzymes by cytotoxic poisons, acidosis (at diabetic and uraemic cоma), ndeficiency of power substances or blockade of their recycling (starvatiohypoglycemis coma). In development of brain hypoxia disorders of nmicrocirculation play role. Owing to hypoxia it is broken oxidizing nphosphorelation, the content and use АТP and ncreatinphosphate decreases.

2. nInfringement of synaptic transmission to the central nervous system. They may nbe connected with:

a) ninfringement of synthesis, transport, deposition and secretion of nneuromediators;

b) nreplacement of neuromediators by pseudomediators;

c) nexcessive activation of inhibition postsynaptic receptors;

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

3. nInfringement of electrolyte balance with changes of cellular potentials and nprocess of polarization of neurons membranes, and also infringement of osmotic npressure. Disorders of metabolism of K, Ná, Mg, Са nin a combination with infringements of the acid-base balance (diabetic, nuraemic, chlorinehydropenie, hepatic etc. comas) have the greatest value.

4. nChanges of physical properties and structures of brain and intracranial nformations. Pathogenetic value has swelling and edema of brain and braimembrane, increase of intracranial pressure which strengthens infringement of nhaemodinamics and liquordynamic, make hypoxia of nervous cells heavier and noppress their physiological activity. Mechanical damage of brain matters cells nat a craniocerebral trauma, tumours, hemorrhage in brain. At separate kinds of ncomas whom each of the listed factors may have leading mean, however they act ntogether more often. At deep coma disorders of regulation of vegetative nfunctions result in addition in heavy infringements of metabolism in aorganism, including brain, and create vise circle in pathogenesis of coma.