DISORDERS OF VASCULAR FLOW: EDEMA, CONGESTION,
HEMORRHAGE, THROMBOSIS, EMBOLISM.
survival of cells is dependent on the oxygen provided in a normal blood supply
 -disorders of blood supply and exchange of fluid cause some most commonly
encountered disorders in medicine: edema, congestion, hemorrhage, shock,
and three interrelated conditions: infarction, thrombosis, embolism.
 -thrombosis, embolism and infarction underlie the most important diseases
and immediate causes of death in industrialized countries: myocardial
infarction, pulmonary embolism, brain strokes
 EDEMA
Edema= abnormal accumulation of abnormal amounts of fluid in the intercellular
space or body cavities
Edema may be
-localized
-generalized
Severe and generalized edema, producing marked swelling of the subcutaneous
tissue = anasarca
edematous collection of fluid in body cavities :
hydrothorax - chest cavity
hydropericardium - pericardial cavity
hydroperitoneum (ascites ) - abdominal cavity
-noninflammatory edema-is called transudate- low amount of proteins
 pathogenesis of edema:
major factors in a pathogenesis of edema -intravascular
hydrostatic pressure and plasma osmotic pressure -have
opposing effects
-Normal state= hydrostatic pressure at the arterial end of capillary is higher
than colloid osmotic pressure, on the other hand hydrostatic pressure in venous
ends of capillaries is lower, thus fluid leaves at the arterial end and returns at
the venous end of capillary, the rest is drained by lymphatics to be returned
back to the bloodstream.
Major primary causes of non-inflammatory edema:
1.- increased hydrostatic pressure in veins -may result of impaired venous
outflow, caused for example by thrombosis- most common in legs- thus localized
edema
generalized increase in venous pressure- occurs in right-sided congestive heart
failure
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2.- reduced osmotic pressure- results from the excessive loss or reduced
synthesis of serum albumin.
- plasma protein loss- nephrotic syndrom (increased permeability of
glomerular membranes)
- decreased synthesis of plasma proteins- in liver cirrhosis, in severe
malnutritions
3.- lymphatic obstruction - impaired lymphatic drainage results in
lymphedema (due to obstruction-inflammatory, neoplastic)
filariasis-parasitic infection- often causes massive fibrosis of the
lymph nodes and lymphatic channels- excessive lymphedema of legs and external
genitalia= elephantiasis
cancer of the breast- sometimes treated by removal of axillary
lymph nodes- this may cause severe postoperative edema of the arm
4.- sodium retention -water retention
in acute reduction of renal function- in acute renal failure
 MORPHOLOGY OF THE EDEMA
changes are evident grossly, edema is encountered most often at three sites=
lower extremities, lungs, brain
 subcutaneous edema of the lower extremities- manifestation of heart failure
(of right ventricle)- legs are subject to the highest hydrostatic pressures.
Distribution of edema fluid in heart failure is influenced by gravity, it is termed
„dependent„
 edema in acute renal failure-results of proteinuria and sodium retention,
tends to be generalized, more severe than cardiac edema, affects all parts of
the body equally, manifests mostly in loose connective tissue matricesperiorbital edema
 pulmonary edema-is a prominent feature of left ventricle heart failure,
alveolar spaces are filled with eosinophilic fluid
 edema of the brain- is encountered in a variety of clinical circumstances, such
as brain trauma, meningitis, hypertensive crisis
CLINICAL CORRELATIONS
edema may be lethal-for example: edema of the lungs- impaires normal
ventilation- (alveolocapillary block )- may result in cardio-respiratory failure
edema of the brain- clinically serious - may cause death
edema of legs or minor forms of renal edema- do not cause severe clinical
difficulties, but important indicator for diagnosis of underlying disease
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 HYPEREMIA OR CONGESTION
congestion= local increase of volume of the blood - caused by dilatation of the
small vessels
active hyperemia:
-results from an augmented arterial inflow
occurs for example - in muscles during exercise
- in inflammation
passive hyperemia:
-results from diminished venous outflow
occurs for example - in cardiac failure
- in obstructive venous disease
chronic passive congestion is always accompanied by edema
- chronic passive congestion and edema of the lungs, one of the most reliable
indicators of left ventricular cardiac failure
- chronic passive congestion of the liver, kidney, spleen -represents an indicator
of right ventricular failure
 HEMORRHAGE
= hemorrhage results from rupture of a blood vessel
-rupture of large artery or vein- caused by some type of injury, such as
trauma, atherosclerosis, inflammatory or neoplastic erosion of a blood vessel
wall
-rupture of small arteries-in systemic diseases
hemorrhagic diathesis = increased tendency to hemorrhage
Hemorrhages may be -external-may cause exsanguinating
- internal- is referred to if blood is trapped in tissues
hematoma= general term for hemorrhage
hematoma may be even lethal- rupture of abdominal aorta in a dissecting
or atherosclerotic aneurysm-massive retroperitoneal hematoma
petechiae= minor multiple hematomas in the skin, mucosal and serosal surfaces
purpura= multiple slighty larger hematomas
ecchymoses= large subcutaneous or subserous hematomas (more than 1-2 cm in
diameter)
blood collection in body cavities:
hemothorax= the blood accumulates in pleural cavities
hemopericardium= in pericardial cavity
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hemoperitoneum
hemarthros
CLINICAL SIGNIFICANCE:
-depends on the volume of blood lost by hemorrhage and on the site of
hemorrhage
larger and acute blood loss - may cause posthemorrhagic shock
site- when located in brain- even smaller hemorrhage may cause death
repeated external hemorrhages- may result in severe lack of iron- iron
deficiency anemia
 THROMBOSIS
thrombosis=
thrombus
formation of clotted mass of blood,
the clotted mass itself=
thrombus may flow downstream in blood vessel system= embolism
the process of clotting and embolism- closely related= thromboembolism
 pathogenesis of thrombosis =inappropriate activation of normal hemostasis
Normal hemostasis: three major contributing aspects of normal hemostasisplatelets, endothelial cells and coagulation system
-1- intact endothelial cells serve to protect blood platelets and
coagulation protein from highly thrombogenic subendothelial substance
(collagen)
- injury to endothelial cells represent a loss of anticoagulative mechanism
- endothelial injury- the most important influence in thrombogenesis in arteries
-thrombi appear often on ulcerated atherosclerotic plaques in arteries, at
sites of inflammatory or traumatic injury to arteries, in arteries whose walls
have been infiltrated by cancer
-thrombi appear regularly in heart chambers adjacent to myocardial
infarct due to hypoxic injury to endocardium
-2- stasis and turbulence of blood - constitutes major thrombogenic
influence in veins
-in normal blood flow- all blood cells are separated from the endothelial
surface by a plasma zone devoid of cells
- stasis and turbulance and decrease of rate of blood flow result in:
1.- erythrocytes and platelets come to contact with endothelial cells
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2.- permits the formation of platelets aggregates and fibrin often in pockets of
stasis
3.- prevents dilution of clotting factors in plasma
4.- decreases inflow of clotting factor inhibitors
5.- promotes endothelial cell hypoxia and injury
Stasis play dominant role in thrombosis in veins because of low speed of
blood flow in veins - origin of venous thrombi in sinuses behind venous valves in
deep vein in low extremities
similar phenomenon- in auricular appendices of heart chambers - in atrial
fibrillation
- stasis and turbulence contribute to thrombosis in arterial aneurysmal
dilatations
-3- hypercoaguability of the blood -is defined as alteration of the
blood and the clotting mechanism that predispose to thrombosis- is called
thrombotic diathesis
rare- good example is inherited lack of natural anticoagulant antithrombin IIIpatients suffer of recurrent thromboembolic attacks
thrombotic diathesis in several chronic diseases - such as
- nephrotic syndrome
- late pregnancy
- disseminated cancer
- use of intraoral contraceptives- increase in plasma level of prothrombin,
fibrinogen and other coagulative factors can be demonstrated
-trauma, surgery, burns
-cardiac failure
-advanced age, immobilization and reduced physical activity increase the risk of
venous thrombosis
 MORHOLOGY OF THROMBI
-thrombi may develop in any part of cardiovascular system (heart, veins,
arteries, capillaries)
-arterial and cardiac thrombi: arise at sites of endothelial injury,
atherosclerosis- often at the site of branching of the artery- white or mixed
thrombi- composed of fibrin white blood cells and erythrocytes
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-mural thrombus- thrombus attached to one wall of the artery- mural
thrombi also develop in abnormally dilated arteries-aneurysms
-occlusive thrombi
smaller arteries
- thrombus completely obstructs the lumen-
in
most commonly affected arteries: coronary, cerebral, femoral, iliac, mesenteric,
popliteal
-venous thrombi: also known as „phlebothrombosis„- mural or occlusive
-in slower-moving blood in veins- red coagulative or stasis thrombi composed mostly of fibrin and erythrocytes
most commonly affected veins: veins of lower extremity (deep calf, femoral,
popliteal, iliac), periprostatic plexus, portal vein etc
venous thrombi can be confused with postmortem clots at autopsy
postmortem clots- are not attached to the endothelial surface, are
rubbery and gelatinous, have smooth surface, do not contain platelets
in contrast, thrombi are more firm, almost always have point of
attachment, on the section show barely visible strands of fibrin
areas of attachment are characteristic for thrombi -frequently the attachment
is most firm at point of origin of thrombus
the tail of thrombus may not be attached- in arterial circulation-the tail builds
up retrograde to direction of blood flow, on the contrary in veins, the tail
extends in the direction of the blood flow
the tail is only loosely attached in veins- its fragments readily creates emboli
-heart valvular thrombi : thrombi may be deposited on heart valves- only
in special circumstances- blood-borne infections may attack heart valvesendocardial damage- associated with development of thrombus - in bacterial or
infective endocariditis
less commonly- verrucous endocarditis-appear in patients with systemic lupus
erytemathodes- autoimmune complex disease affecting skin, kidney and other
organs
nonbacterial or thrombotic endocarditis - in older patients with terminal cancers
or severe malnutrition-marasmus
= marantic endocarditis- hypercoagulative state + minor endocaridial injury are
leading pathogenetic aspects
 ORGANIZATION OF THROMBUS:
1.- thrombus may continue to grow into adjacent vessels
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2.- thrombus may embolize
3.- thrombus may be removed by fibrinolytic activities
4.- it may undergo organization- when thrombus persists in situ for several
days- it may be organized= ingrowth of granulation tissue and mesenchymal cells
into the fibrinous thrombus
-thrombus is populated with spindle mesenchymal cells and capillary
channels are formed within thrombus
-the surface of thrombus becomes covered by endothelial cells
capillary channels anastomose- recanalization = reestablishing the continuity of
original vessel
 CLINICAL SIGNIFICANCE of thrombosis:
1. they cause obstruction of arteries and veins and may lead to infarction
2. they may provide the source of embolism
most important arterial thrombi- myocardial infarction (coronary artery
involved) or cerebral infarction (brain artery involved)
most venous thrombi are occlusive-the great preponderance in veins of lower
extremity,
-superficial veins-varicosities, such thrombi may cause local edema and
congestion and pain, rarely give rise to emboli, local edema predispose to
infection-varicous ulcers difficult to heal
-deep veins of the leg (popliteal, femoral, iliac)- the most important
source of emboli, they also may cause edema, pain, tenderness but approximately
half of the patients with deep vein thrombosis are asymptomatic
 high risk patients for arterial thrombosis:
-arterial thrombi are most likely to develop in patients with myocardial
infarction, with atherosclerosis of the aorta and large arteries with ulcers of
atherosclerotic plaques, rheumatic heart disease, arterial aneurysms
In myocardial infarction- alteration in heart contraction, endocardial damage,
stasis of blood indilated heart chambers most often in auricular parts (dilated
atrium and atrial appendices)
-fragments of arterial thrombi may cause emboli to such sites as brain,
spleen, kidney, the legs, etc.
 EMBOLISM
Embolism refers to occlusion of some part of the cardiovascular system by the
impaction of embolus transported to the site of occlusion by the blood stream.
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- most emboli represent parts of thrombi, thus the term thromboembolism,
-much less commonly-other material such as fat droplets, gas bubbles,
atherosclerotic debris, tumor fragments, etc
 TYPES OF EMBOLISM:
1. pulmonary embolism
2. systemic embolism
3. paradoxical embolism
PULMONARY EMBOLISM: most common example of embolism- thrombus
originates in venous system of legs, especially of deep leg veins, occasionally
from right side of heart and embolus or emboli are transported into right heart
ventricle and to pulmonary arteries
pulmonary emboli may have various forms:
-multiple small emboli in peripheric branches of pulmonary artery
-large snake-like emboli
-saddle embolus-massive embolism in main pulmonary artery
morphologic and functional consequences of pulmonary embolism depend on the
state of pulmonary circulation and the size of affected artery :
-large emboli impact in main pulmonary arteries-death usually follows
suddenly from hypoxia or right ventricle heart failure (acute cor pulmonale) no time to develop morphologic changes in lung tissue
-smaller emboli impacted in medium-sized arteries- pulmonary hemorrhage if pulmonary circulation is normal, the vitality of
lung tissue is maintained, but alveolar spaces are usually filled with erythrocytes
- hemorrhagic infarction if pulmonary circulation is compromised, such as
in congestive heart failure. Pulmonary infarction is sharply circumscribed
necrosis of triangular shape with apex pointing towards the hilus of the lung,
pleural surface is covered with fibrinous exudate
 CLINICAL COURSE OF PULMONARY THROMBOEMBOLISM:
-many pulmonary emboli are clinically silent- small embolic mass is rapidly
removed by fibrinolysis, or larger one may be subject of healing = organization
of emboli - result in postembolic recanalization - healing
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-recurrent multiple emboli= successive thromboembolism- may cause
chronic hypertrophy of right ventricule and right-sided heart failure- chronic
cor pulmonale (pulmonary hypertension and chronic right ventricle failure)
-embolic obstruction of middle-sized arteries- not infarction, but foci of
hemorrhages- hemoptysis and dyspnoe
-obstruction of small peripheral arteries- usually cause infarctions
-massive pulmonary embolism-acute heart failure-sudden death
 SYSTEMIC EMBOLISM - is a embolism to systemic arteries, most commonly
affected organs are - brain, kidney, spleen
Sources of emboli for systemic embolism:
- intracardiac mural thrombi ( in myocardial infarction)
-atherothrombotic fragments from the aorta and the large arteries
-thrombi from the heart valves
-left heart atrium - in atrial fibrillation
- thrombi from left ventricle aneurysms
 PARADOXICAL EMBOLISM - is embolization from systemic veins to
systemic arteries most common source- clots in deep leg veins
abnormal opening between right and left atrium (foramen ovale) combined with
higher blood pressure on right side than on left allows
most common target organs- arteries of the brain, kidney, spleen
 FAT EMBOLISM = is lodgment of fatty droplets and minute globules of fat in
blood capillaries
fat embolism appears as a complication of bone fractures -fragments of fatty
bone marrow, soft tissue traumas and burns
-about 90% patients with severe skeletal injuries have fat embolism, but
very few have clinical course known as fat embolism syndrome -acute respiratory
insufficiency, neurological symptoms, anemia and thrombocytopenia - syndrome
appears about 2 - 3 days after injury
-the fat embolism syndrome has mortality of about 10%
 AIR EMBOLISM ( including CAISSON DISEASE )
= is defined as entry of air bubbles into venous or arterial blood vessels
-in venous air embolism- small quantities are innoculous, but 100 ml and
more may be fatal
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-in arterial air embolism- even small quantity may be fatal, most commonly
occurs as complication of abortion, chest surgery
caisson disease is a distinctive form of gas embolism =decompression sickness
-may appear in deep sea divers who ascend rapidly to high altitudes
-the gases within pressurized air are dissolved in the blood, tissues and
fat, if the diver then ascends up rapidly to the surface- the dissolved oxygen,
nitrogen and carbon dioxide come out of solution in the form of small bubbles
-the most dangerous seems to be nitrogen, because of its low solubilitynitrogen persists as gas bubbles
The formation of bubbles of nitrogen- mainly in the brain - it may induce focal
brain necroses
the same process may affect other highly vascularized tissues and organs, such
as heart and kidney, skeletal muscles, etc.
in the lungs- sudden respiratory distress syndrom
TREATMENT: rapid placing of the affected person into the compression
chamber- and slow decompression
 AMNIOTIC FLUID EMBOLISM -is characterized by sudden onset, rapid
dyspnea, cyanosis, collapse and coma with convulsions
-occurs rarely, is totally unpredictable, may be fatal - is one of major causes of
maternal death after delivery
typical findings:
-in pulmonary arteries and capillaries- epithelial squames from fetal skin,
lanugo hairs,
-fibrin thrombi indicative of DIC - in small vessels of uterus, lungs,
kidney, thyroid, myocardium
-the main cause of DIC syndrome is infusion of amniotic fluid into the
blood, via cervical uterine veins, from the uteroplacental site , etc
- vasoactive substances from the amniotic fluid are responsible for pulmonary
vasocontriction and thrombogenic substances from amniotic fluid cause
intravascular coagulation leading to DIC
 DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
= is characterized by activation of coagulation sequence that leads to formation
of multiple minute fibrin thrombi in capillaries and small venules
-the thrombi are mostly composed of fibrin and aggregations of platelets
10
this leads to widespread thromboses with consumption of platelets and of
coagulation factors and with subsequent fibrinolysis (secondary effect)
-thromboses cause focal ischemia - multiple foci of necrosis (lungs,
kidneys, brain, heart)
-increased bleeding tendency causes multiple hemorrhages
main clinical disorders associated with DIC:
DIC is not primary disease, it is a complication of several underlying diseases,
such as
-amniotic fluid embolism
- EPH gestosis
- septic abortion
-retained dead fetus or abruption of placenta
-severe infections (gram-negative sepsis for example)
-neoplasms, such as carcinoma of pancreas, prostate, lungs
-massive tissue injury, burns
-extensive surgery, etc
 morphology of DIC:
-widespread occurrence of fibrin thrombi in capillaries of kidney, adrenal
glands, brain, and other organs
-ischemia and multiple microinfarcts- necrosis in adrenals may cause
Waterhouse-Fridrichsen syndrom
necrosis in brain- severe neurologic complications
DIC leads to hemorrhagic diathesis, because of consumption of
clotting factors in multiple microthrombi
increased bleeding tendency - multiple hemorrhages
INFARCTION. SHOCK
 INFARCTION
-infarct is a localized ischemic necrosis in an organ or tissue resulting from
sudden occlusion of arterial supply
CAUSES OF INFARCTIONS:
-thrombotic or embolic occlusions11
1. thrombosis = in situ formation of the blood clot that occludes the lumen
of the blood vessel
2. embolism = a portion of the thrombus in one area breaks off and lodges
into the blood vessel of the other area usually of narrower lumen
less common causes of infarcts include:
3. atherosclerosis = narrowing of lumen or the total obstruction of the
lumen by atherosclerotic plaque alone- due to ulceration, hemorrhage, or edema
of the plaque
4. spasm of artery = due to active pathologic vasoconstriction
5. hypotension - causes severe temporary impairments of blood supply in
an area of compromised circulation
6. twisting of the blood vessel with occlusion of both arteries and veins
-in a hernial sac or under peritoneal adhesion
-in cases of torsion of organs or tissues that have the blood supply
through a pedicle, such as ovaries, testes
7. pressure of blood vessel - caused by expanding tumor or due to
mechanical pressure in decubital ulcer
 MORPHOLOGY OF INFARCTS:
Infarcts can be divided into two types:
-white (anemic)
-red (hemorrhagic)
the distinction is given only by amount of hemorrhage that occurs in necrotic
area, the difference is not principal
1. WHITE, PALE INFARCTS
- in solid organs (heart, spleen, kidney)- firm consistency of the organ
does not permit blood inflow into the necrotic area
2. RED, HEMORRHAGIC INFARCTS
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- in loose, spongy tissues (lungs, intestine) permits blood to collect in
necrosis from the anastomosing capillary circulation -hemorrhagic infarcts are also encountered if the venous outflow from
the necrotic area is limited -for example hemorrhagic venous infarction of
intestine
-in some instances, spasm of vessels about clot subsequently relaxes
causing partial hemorrhagic infarction
all infarcts ( white and red )- tend to be wedge shaped, occluded vessel is at the
apex of necrosis and the periphery of the organ forming the base of infarct
-the adjacent serosal surface is covered with fibrinous exudate
 MORPHOLOGY OF DEVELOPING INFARCT:
1- at the onset- all infarcts tend to be poorly defined and slightly hemorrhagic
due to anoxic leakage of residual blood from capillaries in affected area - early
infarcts are grossly red
2- at later stage- white infarcts in solid organs- (spleen, kidney) become well
circumscribed, progressively pale, sharply delimited with hyperemic border -hemorrhagic infarcts in spongy organs - (lung, intestine), first
the infarct is cyanotic, later is firmer and brown (hemosiderin deposits), the
delimitation of infarcts- inflammatory reaction and hyperemia at the margins of
necrosis
-in organs with excellent collaterals- the infarction remains red because
blood continues to be poured to the affected area
-in venous occlusion- infarction is usually hemorrhagic
-in heart- appearance may be mixed red and white, yellow color is due to
accumulation of leukocytes
-in brain- cerebral infarction usually undergoes liquefaction
3- at last stage -in most organs, the infarcted area is replaced by granulation
tissue which is finally replaced by a scar with deposits of hemosiderin
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-in lungs- infarcts dry out, become paler eventually are replaced by scars
-in heart - a similar phenomenon occurs, but solid consistency of heart
muscle does not permit great shrinkage and even prominent scar is of normal
size (myofibrosis)
-in brain- scars do not appear in the brain, and the necrotic area liquefies.
As a result, a pseudocyst may be formed- smooth-walled, glia-lined cavity
(postmalatic pseudocyst)
-in intestine- infarction causes death if not removed surgically- no
development
 FACTORS THAT INFLUENCE THE DEVELOPMENT OF INFARCT
 1- nature of vascular supply
-the most important is an availability of alternative way of blood supply in
the affected area - role of collateral circulation
-in organs with abundant collateral circulation (notably the lungs)- arterial
occlusion leads to development of infarct only if preexisting vascular disorders
(usually congestive heart failure) is present
the lungs have dual arterial supply (pulmonary system and bronchial
arterial supply)
-occlusion of small branch of pulmonary artery in young person with
normal bronchial circulation does not produce infarct
-embolism in older person with pulmonary hypertension and pulmonary
congestion, emboli often result in hemorrhagic infarcts
in liver- similar situation with dual circulation- hepatic and portal
arterial system
upper extremity-double arterial supply through radial and ulnar
arteries- of the hand and forearm- prevents development of infarction or
gangrene of this extremity, this is not true for legs
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heart- collateral circulation- may operate even in coronary
circulation- important in preventing myocardial infarction
-three major coronary arteries (left anterior descending, left
circumflex and right coronary artery)- effective small anastomoses between
these three trunks
 2- rapidity of occlusion
-slowly developing occlusions-usually cause vascular atrophy, very seldom
cause infarct - since they provide opportunity to improve or develop the
alternative blood supply,
-rapidly developing occlusions-more likely to cause infarct
 3- vulnerability of tissue to hypoxia
the susceptibility of a given tissue to hypoxia influence the likelihood of
infarction
neurons and nervous tissue- irreversible damage even after 4-5 min
of anoxia
myocardial cell also very sensitive to hypoxia
in contrast, less sensitive are fibroblasts, adipocytes, skeletal
muscle
many epithelial cells- resistant to hypoxia
 4-oxygen-carrying capacity of blood
patients with normal levels of oxygen transport tolerate better disorders of
vascular supply, than those with anemia or cyanosis
-thus, cardiac failure can contribute to development of infarct through
reduced level of oxygen transport capacity
 SHOCK
= acute circulatory deficiency caused by inadequacy or maldistribution of blood
supply resulting in circulatory hypovolemia
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-may develop following any massive insult to the body, constitutes a
widespread hypoperfusion of cells and tissues due to reduction of blood volume
or due to redistribution of blood resulting in a considerable decrease of
effectiveness of circulation.
-leads to serious tissue ischemia, irreversible injuries and may eventually
cause the death of patient
 TYPES OF SHOCK:
1. - CARDIOGENIC = shock related to cardiac pump failure
-caused by heart muscle damage (myocardial infarction, rupture of heart),
or
rhythmic
disorders,
(arrhytmias),
and
pulmonary
embolism,
cardiac
tamponade, etc.
-HYPOVOLEMIC- results from either internal or external fluid loss
-both hypovolemic and cardiogenic shock cause a drop in cardiac output and a
decrease in tissue perfusion
2.- HEMORRHAGIC SHOCK
-blood loss may be - external or internal
-may be initiated by trauma or endogenous (spontaneous) resulting from
ulcerating or necrotizing lesions, such as- disruption of artery wall in peptic
ulcer
-bleeding from arteries due to tumor invasion
-bleeding from varices- esophageal in liver cirrhosis
-from dissecting or saccular arterial aneurysm
-fluid loss (excessive vomiting, diarrhea, burns)
 - BURN SHOCK= massive loss of fluid and blood cell into injured tissue and
from denuded surface
-Mechanisms underlying cardiogenic and hypovolemic shock-low
cardiac output, hypotension, decreased tissue perfusion, tissue hypoxia
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3.- SEPTIC = shock related to severe bacterial infections, (particularly gramnegative bacilli, such as Escherichia coli, Klebsialla pneumoniae)gram-positive bacteria, such as streptococci, pneumococci
-endotoxemia secondary to sepsis causes increased vascular permeability
and internal loss of fluids from the circulation
Mechanisms underlying septic shock less obvious - in majority of cases endotoxins and DIC are most important in pathogenesis.
 ENDOTOXIC SHOCK
-cardiac output is not lower, but the capacity of arterial system is abnormally
incresed due to arterial dilatation
-septic shock is associated with defects of distribution of blood- so called
peripheral pooling, with endotoxin-mediated activation of inflammatory response
and direct toxic damage to the tissues
4-NEUROGENIC - after anesthesia, and in spinal cord injury
major mechanism is peripheral vasodilatation with pooling of blood
 PATHOLOGY AND PATHOGENESIS OF SHOCK :
-whatever the main cause leading to shock is, major pathogenetic aspect
is diminished volume of circulating blood
-due to loss of extracellular fluid or due to blood loss
-due to pooling of blood in certain areas, such as in the abdominal
viscera in abdominal trauma
 STAGES OF SHOCK:
1- non-progressive stage-reflex compensatory mechanisms are activated
and perfusion and blood supply to vital organs is preserved
2- progressive stage -is characterized by tissue hypo-perfusion,
progressive tissue hypoxia due to arterial dilatation and stasis, function of vital
organs begin to deteriorate- the patient is confused
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3- irreversible stage - is characterized by irreversible tissue injury of
hypoxia, condition no longer responsive to therapy
-the flow through the renal cortex is markedly reduced - renal tubular necrosis
develops, with consequent decrease in the urinary output- resulting in metabolic
acidosis
 MORPHOLOGIC CHANGES DUE TO SHOCK:
-tissue changes are essentially the same as those of hypoxic injury,
-late stages of shock are characterized by failure of multiple organs
brain-ischemic encephalopathy- changes due to ischemia and hypoxia -changes
depend on the duration of hypoxia
-in mild cases- transient confusional state, more severely affected
patients will be comatose with subsequent loss of part of cortical function
heart -variety of changes- myocardial infarction, subendocardial hemorrhage,
lungs- so called shock lung - Adult respiratory distress syndrome ARDS,
-ARDS is a clinical syndrome not always but often associated with shock,
-grossly. the lungs are firm, dark red, airless, heavy
-microscopically: capillary congestion, intra-alveolar edema and hemorrhage,
fibrin thrombi may be present in capillaries, diffuse alveolar damage, hyaline
membranes lining the alveolar surfaces,
kidneys-acute tubular necrosis
adrenal glands- focal depletion of lipids in the cortical cells-this loss of
corticolipids does not imply adrenal exhaustion, but more likely activated state
and increased production of corticoids
gastrointestinal tract -focal mucosal hemorrhages
liver-fatty change or centroacinar necroses
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