Download Haemodynamic disturbances

*Haemodynamic disturbances
*Venous congestion
*Oedema
*Bleeding
*Pathological thrombosis
*Embolism
*Ischemia & Infarction
*Shock
Venous congestion :accumulation of blood in the
venous site of the circulation due to obstruction of
the venous return.
It cause bluish discoloration of skin due to
accumulation of stagnated blood contianing deoxygenated hemoglobin
and it should be
differentiate from other term which is hyperaemia
which is also increase in the amount of blood in the
artierioles of the affected tissue or organ but it is
an active process due to neurogenic mechanism
cause arteriolar dilitation and local redness due to
accumulation of oxygenated blood e.g acute
inflammation.
I-systemic venous congestion:
Here the systemic vein is congested and it is usually
seen in right side heart failure which is due to
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pulmonary valve stenosis or due to diseases of the
lung.
Chronic venous congestion lead to hypoxia which
cause degeneration & necrosis . its effect mainly
seen in the abdominal viscera such as liver .spleen
and kidney.
Structural changes of systemic venous congestion :
In addition to generalized oedema , structural
changes are seen in liver ,spleen and kidney.
In liver grossly it is enlarge ,firm , cut surface show
mottled or nutmeg appearance .
Mic :.
*The central vein & the surrounding sinusiod are
distended with blood (red )
* The surrounding hepatocyte show fatty changes(
pale) . .
* The dark central area surrounded by paler area
producing nut meg liver.
* With time chronic congestion lead to fibrosis in
the centrilobular area associated with hyperplastic
nodule resulting from compensatory proliferation
of the surrounding paranchyma producing cardiac
cirrhosis.
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Spleen become enlarge and firm grossly.
Microscopically Congestion of the sinusoid of the
red pulp which
appear black while the white pulp appear as pale
spot.
2- Pulmonary venous congestion:
Seen in left sided heart failure (due to systemic
hypertention,coronary heart disease ) which lead to
increase pressure in the left atrium and pulmonary
vein ..
Microscopically:
Congestion of the venules and alveolar capillary .
alveolar space filled with RBCs & heamosidrin
laden macrophage(heart failure cell) .
the heamosidrin causing irritation and subsequent
fibrosis of the alveolar wall.
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The condition is called brown induration of the
lung due to associated fibrosis with brown color
of heamosidrin .
3-Local venous congestion:.
Due to mechanical interference with the venous
drainage from an organ or limb could be :
1-acute due to ligation or thrombosis of the blood
vessel .
2-chronic as in fibrosis of b.v wall , pressure from
outside by tumor or organized thrombosis .
Oedema:
Oedema is an abnormal accumulation of fluid in the
interstitial space and it is either generalize or
localize.
Oedematous fluid is either of transudate or exudate.
The transudes (non inflammatoryoedema)
usually contain few cells , with low protien
<3gm/dl and low specific gravity less than 1.010 ,
in contrast to the exudates(inflammatory oedema)
in which the cells are numerous , protein is more
than 3 gm/dl & specific gravity is more than 1.010
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Causes ,pathogenesis of non inflammatory
oedema :
1- Increase in the hydrostatic pressure : as in right
sided heart failure .
2- decrease in the colloid ( oncotic ) pressure : due
to reduction in albumin synthesis or increase in
protein loss as in nephrotic syndrome .
3- Lymphatic obstruction : usually localize due to
inflammation or obstruction by tumour .
4- Sodium & water retention due to impairment in
renal function , both can cause increase in the
hydrostatic pressure & diminish in the oncotic
pressure .
A : Generalized oedema
Causes(types):
1- cardiac oedema: due to sever heart failure :
A: there is reduction in cardiac out put→↓ in renal
flow and glomular filterate rate , so this will
stimulate the secretion of renin which stimulate the
secretion of aldosteron causing retention of Na &
water retention .
B:Could be due to accumulation of waste product
in the interstitial tissue which will rise the osmotic
pressure there so more water is withdrawn from
circulation ..
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C:Chronic hypoxia →↑vascular permeability so
more water and Na will pass outside b.v.
D: Reduction in venous return → increase in the
hydrostatic pressure at the venous end so cause
reduction in the re-entry of fluid to the circulate.
2- Renal oedema:
could be due to :
A-Nephrotic syndrome which is a group of disease
characterized
by
heavy
proteinuria
→hydpoproteinemia that cause generalize oedema.
B- it could be due to disease affect glomeruli as in
acute diffuse glomerularnephritis which have
reduction in renal blood flow and decrease
glomerular filtration rate the cause of which is
unknown and may be due to defect in rennin
angiotension system.
3- Nutritional oedema:
it is seen in sever malnutrition as in kwashiorkor
which could be due to low plasma protein or due to
replacement of subcutaneous fat by loose C.T
causing low tissue tension and enhance the
accumulation of fluid.
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4-Hepatic oedema :
the cause is not well known could be due to
hypoproteinemia.
B: Localized oedema:
1-Acute inflammation : due to increase in
hydrostatic pressure which enhance exudation of
fluid , due to increase in vascular permeability so
protien escape
outside bv so oncotic pressure is reduced and this
enhance the accumulation of blood outside the b.v
2- Local venous obstruction :
physiological as in oedema of the leg follow
prolong sitting without
leg movement OR
pathological due to deep vein thrombosis of the leg
.
3- chronic lymphatic obstruction: as in tumor
press or invade lymphatic wall or due to chronic
inflammation of lymphatic vessel .
4-Pulmonary oedema: cause :
A-due to increase in hydrostatic pressure of
pulmonary circulation as in left ventricular failure.
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B-overloading of circulation as in rapid blood
transfusion in anemic patient.
C-asapart of generalize oedema as in
glomerulonephritis.
D- increase in intracranial pressure as in head injury
.
Heamorrhage:
Extravasations of blood due to rupture of b.v or due
to group of clinical disorder called heamorrhage
diathesis( bleeding tendency ) .
Types of bleeding :
*-bleeding either external .
*-or internal :
-- hematoma : accumulation of blood in the
tissue .
-- Peticheal hemorrhage : minute bleeding (12mm) (due to reduction in platelets number or ,
platelet dysfunction ).
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-- purpura : bleeding (3-5 mm) in the skin , its
causes as above or due to vasculitis).
-- ecchymosis : (1-2cm) bleeding in the skin
which has early red blue color due to accumulation
of (Hb) →blue green (bilirubin)→golden yellow
(heamosidrin).
-- large bleeding may accumulate into body
cavity forming heamoperitonium, haemothorax
haemopericardium.
Effect of bleeding : depend on :
* amount of bleeding .
1- repeated loss of small amount cause iron
deficiency anaemia .
2-rapaid loss of 1/3 or more of blood volume cause
hypovolemic shock.
3- loss of moderate amount ( about 20% ) is liable
for life in healthy person .
* Site: small amount of bleeding which has no
effect if occur in
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subcutaneous tissue may cause death if occur in
the brain .
Pathological thrombosis:
Formation of solid or semisolid mass from blood
constituent within vascular system during life.
The main constituent of thrombi: fibrin ,RBC,
WBC & platelet.
Composition (types ) of thrombi determine by the
rate of blood flow :
1- Pale thrombi: it is seen in artery because of rapid
blood flow, it is firm, pale .
Mic : compose of platelet mainly with fibrin &
some RBC.
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2-Red thrombi: seen in stagnated blood adjacent to
complete occluded blood vessel ,it is soft ,red .
Mic : compose of fibrin strand with large no. Of
RBC in between with little platelet &WBC.
3- Mixed thrombi: seen in slow blood vessel as in
vein.
Causes ;( predisposing factor; pathogenesis of
thrombosis) :
1-Endothelial injury : seen in ulcerated
athermanous plague, abnormal valve of the heart ,
hypertension & arterities . here platelets adhere to
damage surface , release thromboplastin & activate
coagulation cascade to produce thrombosis .
2- Change in blood constituent causing hyper
viscosity state, this is seen in oral contraceptive
,during pregnancy ,extensive
burn , metastatic
tumours, , advance age (cause platelet aggregation),
smoking, or due to mutation of prothrombin gene .
3-Altration of blood flow either due to turbulence
as in atheroma Or due to slowness of blood flow seen
in aneurysm , non contracted myocardium as in M.I ,
hyperviscocity syndrome as in polycythaemia, sickle
cell anaemia that cause vascular obstruction& stasis.
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Morphology of thrombosis :
thrombus occur anywhere in cardiovascular system
, they are variable in
size & shape depend on the site of origin & the
condition predispose to its formation .
Arterial or cardiac thrombus usually begin at site of
endothelial injury or turbulence
while venous
thrombi occur at site of stasis .
All thrombi are firmly attach to the point of origin ,
arterial thrombi grow in retrograde direction from the
point of attachment while venous one extend in the
direction of blood flow to the heart.
Aortic & cardiac thrombi (mural thrombi ): have
laminated appearance called line of zahn produced by
pale layer of platelets & fibrin that alternate with
darker layer containing more RBC .while in venous
thrombi the lines are less apparent & instead it look
like blood clot in a test tube .
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Cardiac thrombus is due to abnormal myocardial
contraction ( as myocardial infarction , arrhythmia ,
cardiomyopathy ) OR due to injury of myocardial
surface as in myocarditis .while aortic thrombi is due
to ulcerated atheromatous plaque or aneurysmal
dilation .
Arterial thrombosis are usually occlusive occur in
coronary, cerebral & femoral arteries & seen in
atheromatous plaque or due to endothelial cell injury
as vasculitis or trauma .
Venous thrombus (phlebothrombosis) almost
occlusive , it create a long cast of the vein lumen &
since it associated with stasis it contain more RBC &
called red thrombus , usually occur in the lower
extremities .
red (venous)thrombus
clot
*dry,friable& firm.
rubbery.
* adherent to b.v wall .
post mortem
- gelatinous soft ,
- not adherent.
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* show vaque strand .
yellow chicken fat over red jelly
of pale fibrin .
-surface show
Thrombosis over heart valve is called
vegetation which may occur on damage valve due to
infection ( as infective endocarditis) or due to
hypercoagulable state (nonbacterial thrombotic
endocarditis ) & less commonly occur in association
with SLE .
Clinical correlation : Thrombus is significant due
to obstruction of b.v or due to formation of emboli .
Arterial thrombi can embolize but its role in
obstruction of cerebral &coronary b.v is much
important.
while venous thrombi can cause obstruction with
distal stasis but its role in embolism is more important
.venous thrombosis usually occur in superficial &
deep vein of the leg .
Superficial vein thrombosis occur in the saphenous
vein causing congestion , pain , swelling & tenderness
along the vein & may lead to skin infection & varicose
ulcer , while embolization is rare .
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while deep thrombosis (DVT)occur in a deep vein
& it is more serious due to embolization
&
obstruction occur early but later disappear once
collateral circulation develop .
DVT occur due to:
1- stasis & hypercogulable state as in heart failure
.
2-Reduce physical activity as advance age with bed
rest .burn ,trauma &
surgery due to reduce milking action of muscle of
the legs.
3- Pregnancy & post partum period due to infusion
of amniotic fluid or hypercoagulability .
.
4 which -Disseminated tumour as in carcinoma of
head of pancrease have a high risk of thrombotic
phenomena.
Fate of thrombosis(result):
1-If small undergo lyses i.e. digestion by plasmin or
proteolytic enzyme of neutrophilis.
2-In occluding thrombi which contain a lot of clot ,
retraction of the clot may occur so new canal will form
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which is lined by endothelial cell result in
recanalization.
3-Organisation & recanalization : this is seen in
arterial thrombi in which we have invasion &
digestion by macrophage following by in growth of
fibrovascular granulation tissue.
4-Calcification in the form of dystrophic
calcification
5-Part of it detached →embolism.
6-Infection of thrombi so it is become friable & part
of it detached → pyaemic abscess or septic
infarction .
Embolism :
An emboli is an abnormal ,undissolved mass carried
by blood stream with subsequent impaction in another
vessel any where in the body & the process is termed
embolism.
Types :
1-thrombotic emboli which is the commonest
(95%) & can be carried by arteries & veins .
*Systemic( Arterial emboli) usually arise from :
a- mural thrombi in the left ventricle following M.I
.16
b- less commonly they may arise from left atrium
as in fibrillation.
c -aortic athermanous plague .
d- vegetation on diseased value .
They can lodge any where in the arterial system &
invariably cause Infarction Usually in the lower
extremity , brain , kidney & spleen.
*-Venous emboli (pulmonary embolism ), they
usually originate from deep vein thrombosis ( D.V.T )
of the leg , it then pass to the right side of the heart
& then to the lung:
--Majority are asymptomatic .
-- large emboli can settle at the pulmonary artery
bifurcation or large
artery & may cause death or right side heart
failure .
--smaller emboli will produce pulmonary infarction
or pulmonary hemorrhage .
-- very rare venous emboli may pass to the systemic
circulation through a defect in the heart septum &
called paradoxical embolism.
2-Fat embolism :characterized by progressive
dyspnoea ,convulsion & sometime renal failure
develop 24-72 hrs after sever compression to the
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adipose tissue or bone fracture, here fat droplet enter
ruptured blood vessel at the site of trauma &
deposited at
the cerebral ,pulmonary & renal
vasculature cause occlusion.
3-Air embolism : can occur when air enter large
vein following lung, chest or neck injury . smaller
quantities usually dissolve in the plasma.
Caisson disease occur when deep sea diver is
brought up rapidly to the atmospheric pressure so
nitrogen gas which was dissolve under high pressure
is released in the plasma form numerous small gas
bubbles which obstruct blood vessel throughout the
body produce characteristic joint & muscle pain .
4-Amniotic fluid embolism :occur in prolong or
traumatic labour .
5-Malignant tumor emboli : causing secondary
metastasis .
6-Parasitic emboli.
Ischemia :
It is inadequate blood supply to an area of a tissue.
Causes of ischemia :
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1- 99% it result from thrombotic or embolic
mechanism .
2- complicated atheroma . i.e. atheroma with
subsequent hemorrhage.
3-twisting of blood vessel.
4-compression from out side by tumor or by
entrapment in a hernial sac.
5- venous obstruction can occur in a varicose vein.
Effect of ischemia:
Variable depend on the adequacy of collateral
circulation , if a good
collateral is present it will produce little or no
effect but if the collateral circulation is poor, it will
lead to functional disturbances or even cell death.
Ischemia in the heart can lead to chest pain (angina)
, while in lower limb ,it produce intermittent
claudication (pain in the calf muscle during exercise )
.
Infarction :
An area of ischemic necrosis caused by occlusion
of arterial supply or
venous drainage in a particular tissue .
Causes: same as ischemia.
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Types : (morphologic appearance)
It is either red or pale.
Red infarction usually follow venous occlusion :
* in loose tissue such as lung that allow blood to
collect in infarcted area .
* in tissue with dual circulation such as lung ,
intestine .
* when flow is re-established to a site of previous
arterial occlusion & ischemia e.g fragmentation of
occlusive emboli.
The color reflect the amount of blood which
accumulate in the parenchyma during necrosis.
pale infarction occur due to arterial occlusion in
solid organ (heart ,spleen .kidney) &the solidity of the
organ limit the amount of hemorrhage.
Septic infarction : occur when bacterial vegetation
from heart valve embolize , or when microbes infect
area of necrotic tissue . here infarction convert to an
abscess.
Grossly :
Infarction has a wedge shape , the apex at the site of
occluded blood vessels & the periphery of the organ
forming the base which is poorly define .
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With time the edge become more defined by a
narrow zone of hyperemia due to inflammation & pale
infarction become more paler & sharply defined while
red infarction it become more firm & brown.
Microscopic feature:
* the histological features is that of coagulative
necrosis with the exception of the brain which show
liquefactive necrosis .these changes seen 12 hr- 18hr
after the onset .
* within 1-2 days evidence of acute inflammation
become prominent.
*this is followed by stage of healing by granulation
tissue which end in scar tissue in most of
infarction.
Susceptibility of tissue to ischemia : (Factors that
influence the development of infarction) :
The consequence of vascular occlusion can range
from no or little effect, to death of tissue or even the
individual. In general the extent of infarction is
usually less than that of tissue supplied by that
occluded artery . it depend on:
1- nature of vascular supply. The size of
infarction depend on whether the collateral
circulation are healthy and capable of dilation..
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So tissue which has duel blood supply as the lung
or intestine are relatively resistant to necrosis.
2- The capability of tissue to withstand
ischemia: neuron suffer from infarction if blood
supply is deprived for 3 minutes while cardiac
muscle can withstand hypoxia up to 20-30
minute in contrast to fibrous , fatty and bone
tissue which are less susceptible to ischemia.
3- Rate of development of occlusion: slowly
developing occlusion are less liable to cause
infarction.
4-Oxygen content of blood: partial occlusion of
small vessel in anemia or cyanotic patient may
lead to infarction
Shock:
heamodynemia change result from inadequate tissue
perfusion due to acute fall in cardiac output . At the
beginning these changes are helpful in maintaining
the blood supply to the vital organ such as (heart
and brain) by reducing the blood supply to other
tissue of the body. However if the Cardiac output is
not corrected it will cause damage to the cells of
vital tissue lead to multiple organ failure.
Types of shock and causes:
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1- Cardiogenic shock: it is due to acute cardiac
insufficiency as in M.I., sever myocarditis,
cardiac surgery.
2- Hypovolaemic shock: it is due to reduce in
blood volume as in sever bleeding, extensive
vascular exudation as in burn and condition which
cause dehydration.
If the blood loss is up to 10% it has no effect .
If the blood loss reach 20% lead to significant
hypovolaemia .
If the blood exceed 50% lead to death unless
urgent treatment is given.
3- Septic shock: usually followed sever infection
with septicemia caused by gram negative bacilli
which form endotoxin; as in sever burn,
generalize peritonitis, surgical operation and
instrumentation of urogenital tract. The patient
has generalize features of shock in addition to
fever.
4- Neurogenic shock ;due to anesthetic accident
or spinal cord accident.
5- Anaphylactic shock: cause by generalize IgE
hypersensitivity reaction forming systemic
vasodilation & increase vascular permeability.
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Stages (pathogenesis) of shock and hypovoleamic
shock:
1-An initial compensatory stage during which
reflex compensatory mechanisms occurred to
maintain C.O.P. result in tachycardia, peripheral
vasoconstriction and renal preservation of fluid.
So cardiac output is improved and perfusion of
vital organ is maintain .
2-A progressive stage occur if the underlying
cause is not correct characterized by tissue hypo
perfusion & hypoxia which stimulate anaerobic
glycolysis with execs lactic acid production
lead to lower PH of the tissue with subsequent
vasodilatation and pooling of blood in the
microcirculation lead to decrease C.O.P.
3-Irreversible stage occur if early treatment isn’t
take place and
death occur even if
heamodynamic defect is corrected.
Clinical feature:
Pale, cold, sweaty skin and even cyanosis; rapid
weak pulse, decrease in blood pressure and increase
in rate and depth of respiration. The patient become
restless, confuse and may lead to coma.
Pathological change of shock:
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Shock usually affect the function of the cell.
However it cause swelling of all cell and some time
fatty changes. Different organ involved in shock
including:
1- Lung which show oedema congestion, hyaline
disease, collapse and bronchopneumonia.
2- Liver may show centrilobular necrosis.
3- Kidney may show acute tubular necrosis.
4- stress ulcer in ulcer in stomach .
5- disseminated intravascular coagulation (DIC). (
which
characterize
by
thrombosis
in
microcirculation with subsequent hemorrhage).
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