PATHOPHYSIOLOGY OF
THE
EXTREME
STATES.
PATHOPHYSIOLOGY OF THE
SHOCK.
COLLAPSE.
COMA
EXTREME
STATES.
SHOCK. COLLAPSE. COMA
Professor 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 insertion off 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 life processes basic passes
to a metabolic level. In this stage there are
expressed infringements 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 ethiological 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 infringements 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 (socalled ‘shock lung’) may result in their severe
infringements of gas change functions, similar
changes in kidneys (‘shock kidney’) may lead to
renal insufficiency.
•
•
•
•
•
•
Hemodynamic system disorder:
1. Decrease of volume of circulating blood and
speed of blood flow.
2. Increase of blood deposition, and decrease of
venous return of blood to heart.
3. Fall of tone of arterioles 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 is 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. Turnicate (develops after removal of jute
four hours and more after imposing);
5. Anhydremic (dehydrative);
6. Cardiogenic;
7. Pancreatic;
8. Septic;
9. Infection-toxic;
10. Anaphylactic
after
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
1.
2.
3.
4.
5.
Reduction of volume of circulating blood:
Blood loss (hemorrhagic shock)
Loss of blood plasma at massive exudative
inflammation (burn shock)
Draw of fluid from blood vessels
(anaphylactic shock)
Dehydration (anhydremic shock)
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 - activation of
sympathoadrenal and pituitary-adrenal systems. Absolute
hypovolemia (loss of blood) or relative (decrease of
minute volume of blood and venous return to heart)
results in decrease of arterial pressure of blood and
decrease of baroreceptors activity. As a result of
activation sympathoadrenal and pituitary-adrenal
systems there is secretion of adrenaline and
corticosteroids. Epinephrines would cause consrtiction
of vessels through -adrenoreceptors of skin, kidneys.
Centralization of blood circulation, that is presented by
remaining of blood circulation in vital organs and
pressure in large arterial vessels takes place.
• The second (vasodilating) type directed on elimination
of ischemia. Vasoactive amines are formed, causing
dilation of vessels, increase of their permeability and
disorder of reological properties of blood. Besides there
is a disintegration of cells, activation of proteolytic
enzymes, output from cells potassium ions. There is an
inadequate dilatation of vessels, change of
microcirculation in tissues, decrease of capillary and
strengthening of shunt blood flow, change of reaction of
precapillary sphincters on epinephrines and 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.
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.
Thus, pain stress which is shown by strengthening of
functions of blood circulation system , breath, some
endocrine glands (adenohypophysis, brain and cortex
substances of adrenal glands, neurosecretory nucleus of
hypothalamus) with liberation in blood of excess
quantity corticotropin, adrenaline, noradrenaline,
vasopressin develops.
• The stage of inhibition is more long (from
several hours to about day) and is characterized
by development inhibition processes in the
central nervous system. General inhibition seizes
also the centres of the vital functions (blood
circulation, breath), they are broken, owing to
oxygen starvation develops. Hypoxia, in turn,
aggravates disorder in cardiovascular and
respiratory centres. Disorders of haemodynamic
and external breath progress vice circle becomes
isolated.
•
Hemorrhagic shock appears during external (knife,
bullet wound, erosion bleedings of stomach at stomach
ulcer, tumors, from lung at tuberculosis etc.) or internal
(hemothorax, hemoperitonium) bleedings in conditions
of tissues traumation.
•
Anhydremic shock appears owing to significant
dehydratation at loss of liquid and electrolytes. During
the exudative pleurities, intestinal obturation, peritonitis
liquid comes from vascular system into
cavities.
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’s, 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.
Infringement of contractive activity of heart is
observed also. Sympathoadrenergic reaction thus
is not expressed because of a vascular tone
infringement.
• Collapse, definition, charecteristic.
Collapse is an acute vascular insufficiency is
characterized by fall of a vascular tone and
also acute reduction of circulating blood
volume .
• At the collapse there is a reduction of venous
blood inflow to heart, decrease of heart output,
fall of arterial and venous pressure, infringement
of tissues perfussion and metabolism, hypoxia
of brain appears, the vital functions of an
organism are oppressed. It is shown in clinics
by short-term loss of consciousness.
• 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 conditions may
promote also hypocapnia owing to hyperventilation
• Ortostatic collapse appears at fast transition from
horizontal position in vertical, and also at long time of
standing. Thus there is a redistribution of blood with
increase of total amount of a venous system and decrease
of inflow to heart. In a basis of this condition
insufficiency of a venous tone lays. Ortostatic collapse
may be observed at recovers after heard diseases of
endocrine and nervous system, in the postoperative
period, at fast removal of ascitic liquids or as a result of
spinal and peridural anesthesias. 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. Also
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 strike volume (heart infarction,
infringements of heart rhythm, acute myocarditis
or pericarditis with accumulation of exudation in
cavity of pericardium).
• Pathogenesis: 1) fall of venous and arteriols tone as a
result of action of infectious, toxic, physical, allergic and
other factors directly on a vascular wall, vasomotoric
centre and on vascular receptors (sinocarotid zones,
arches of an aorta); 2) fast reduction of circulating blood
volume (blood loss,plasma loss). Reduction of
circulating blood volume results in decrease of return of
blood to heart by veins of the big circle of blood
circulation and heart output. The blood accumulates in
capillaries, the blood pressure falls, develops circulatory
hypoxia, metabolic acidosis, permeability of vessels
increases. It promotes transition of water and elctrolytes
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 condition
which is characterized by 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 a stage of development of some
diseases. Conducting in their pathogenesis
is defeat of the central nervous system
with infringement 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. They may be connected
with:
• a) disorderof 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 hemodinamics 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.