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Hemodynamic Disorders,

Thromboembolic disease, and


Shock
Edema
- Approximately 60% lean body weight is water, 2/3 of
which are intracellular with remainder in extracellular
compartment (most in the interstitial space)

- Increased fluid in interstitial tissue spaces or fluid


accumulation in the body cavities in excessive amount
is called edema
Depending on the site, fluid accumulation in body
cavities can be variously designated as:
a) Hydrothorax fluid accumulation in pleural cavity in
pathologic amount
b) Hydropericardium pathologic amount of fluid accumulated
in pericardial cavity .
c) Hydroperitoneum (ascites) fluid accumulation in peritoneal
cavity.
d) Ansarca is a severe & generalized edema of the body with
profound subcutaneous swelling.
There are two types of edema
1. Inflammatory edema / Exudate
2. Non inflammatory edema /Transudate
- Inflammatory edema are largely related to local
increases in vascular permeability
- Non inflammatory causes of edema occur in
hydrodynamic derangements
- There are four primary forces that determine fluid
movement across the capillary membrane.
- Each of them categorized under two basic categories,
the hydrostatic pressure & the oncotic pressure.
- These four primary forces are known as STARLING
FORCES.
1. The capillary hydrostatic pressure (Pc)
Which tends to force fluid outward from the
intravascular space through the capillary membrane to
the interstitium.
2. The interstitial fluid hydrostatic pressure (Pif)
Which tends to force fluid outward from the interstitial
space to the intra vascular space.
3. The plasma colloid osmotic pressure (p)
- Which tend to cause osmosis of fluid in ward through
the capillary membrane from the interstitium.
4. The interstitial fluid colloid osmotic pressure
(if)
Which tend to cause osmosis of fluid outward through
the capillary membrane to the interstitium.
- Normally the exist of fluid into the interstitium from the
arteriolar end of the microcirculation is nearly balanced
by inflow at the venular end; a small residuum of excess
interstitial fluid is typically drained by the lymphatics.
Pathophysiologic categories of edema
1.Increased hydrostatic pressure
-.Local increase in venous pressure may result from
impaired venous outflow. E.g. deep venous thrombosis in
lower extremities

-.Generalized increases in venous pressure occur most


commonly in congestive heart failure affecting right
ventricular cardiac function.
2.Reduced plasma osmotic pressure
.It can result from excessive loss or reduced synthesis of
albumin (serum protein most responsible for
maintaining colloid osmotic pressure).
Nephrotic syndrome

Protein malnutrition

Diffuse liver pathology (cirrhosis)


3. Lymphatic obstruction
- Impaired lymphatic drainage leads to localized edema
lymphedema
- It can result from inflammatory or neoplastic obstruction
Filariasis causes massive lymphatic & lymph node fibrosis in
the inguinal region resulting in edema of the external genitalia
& lower limb Elephantiasis
Axillary Lymph node infiltrated by cancer removed by surgery
or irradiatd leads to edema of upper extremity
In carcinoma of breast, infiltration & obstruction of
superficial lymphatics can cause edema of the overlying
skin, giving rise to the so called peau dorange (orange
peel) appearance. It results from an accentuation of
depressions in the skin at the site of hair follicles.
4. Sodium & water retention
- Salt retention can be a primary cause of edema.
- Increased salt , with obligate accompanying water ,
causes both increased hydrostatic pressure &
diminished vascular colloid osmotic pressure.
- Salt & water retention can occur with any acute
reduction of renal function including glomerulonephritis
& acute renal failure
Morphology of edema
- Edema is most easily recognized grossly
- Microscopically it manifests only as subtle cells
swelling with clearing & separation of extracellular
matrix.
- Edema is most commonly encountered in subcutaneous
tissues, the lungs & the brain
Subcutaneous edema
- It can be diffuse or can be more prominent at sites of
high hydrostatic pressures
- Edema distribution typically influenced by gravity is
called dependent
- Dependent edema is a prominent feature of congestive
heart failure, particularly of the right ventricle
Edema as a result of renal dysfunction or nephrotic
syndrome is more severe & affects all parts of the body
equally. Initially it may affect tissues with loose
connective tissue matrix (periorbital edema).

Finger pressure over edematous subcutaneous tissue


displaces the interstitial fluid & leaves a finger-shaped
depression - pitting edema
Pulmonary edema
- It is most typically seen in the setting of left ventricular
failure but it can also be seen in renal failure, , acute
respiratory distress syndrome, pulmonary infections &
hypersensitivity reactions
Grossly, the lungs are two or three times their normal
weight
Microscopically, alveoli filled with frothy, blood-tinged
fluid
Brain edema
- It can be localized or generalized
- Localized (eg abscess or neoplasm), generalized (eg
encephalitis or hypertensive crisis)
- With generalized edema, the brain is grossly swollen,
with narrowed sulci & distended gyri.
Clinical correlation
- The site of edema determines the clinical significance
- Subcutaneous tissue edema is important primarily
because it signals underlying disease
- Pulmonary edema can cause death by interfering with
normal ventilatory function
- Brain edema is serious because if severe the brain can
herniate
Hyperemia and Congestion
- Both indicate an increased volume of blood in a
particular tissue
Hyperemia
- Is an active process resulting from an increased or
augmented tissue inflow because of arteriolar
vasodilation
- Affected tissues become red as there is engorgement
with oxygenated blood.
- Occur in exercising skeletal muscle or acute
inflammation commonly.
Congestion
- is a passive process resulted from impaired out flow
from a tissue.
- Occur systemically as in cardiac failure or locally in
isolated venous obstruction
- Affected tissue appear blue - red due to accumulation of
deoxygenated blood
- Congestion & edema commonly occur together

- In long standing congestion, the stasis of poorly


oxygenated blood causes chronic hypoxia, which can
result in parenchymal degeneration or death
Morphology
Cut surface - hemorrhagic & wet
Pulmonary congestion
1. Acute pulmonary congestion
Alveolar capillaries engorged with blood
Septal edema

2. Chronic pulmonary congestion


Thickend & fibrotic septa
Alveolar space contain hemosiderin laden macrophage, resulting in
brown indurations and pulmonary hypertension
Hepatic congestion
1) Acute hepatic congestion
Central vein & sinusoids are distended
There may be even central hepatocyte degeneration.
Peripheral hepatocytes better oxygenated & developing only
fatty changes
2) Chronic passive congestion of liver
Central lobules grossly depressed because of loss of cells &
appear red brown (NUTMEG LIVER)
Hemorrhage
Definition:
- Extravasations of blood outside the blood vessel.

- Hemorrhage from large vessel is due to vascular injury


including trauma, atherosclerosis, or inflammatory or
neoplastic erosion of the vessel wall
An increased tendency to hemorrhage from usually
insignificant injury is seen in clinical disorders called
hemorrhagic diathesis.
Fragility of blood vessels
Platelet deficiency or dysfunction
Coagulation disorders
- Hematoma - accumulation of blood within a tissue. It
can be trivial or life threatening
- Petechiae - minute 1 to 2 mm hemorrhages to skin,
mucous membranes or serosal surfaces. It is usually
due to low platelet count (thrombocytopenia), locally
increased intravascular pressure or defective platelet
function
- Purpura - larger hemorrhages (>3mm ) that may be
associated with same causes as petechiae or also may
occur secondary to trauma, vascular inflammation
(vasculitis)
- Ecchymosis - larger (> 1 to 2 cm) subcutaneous
hematoma & are characteristically seen after trauma
- Large accumulation of blood can occur in body cavities
& are called hemothorax, hemopericardium,
hemopertonium or hemarthrosis
Clinical significance
- Volume of bleeding
- Rate of bleeding
- Site of bleeding
Hemostasis & thrombosis
- Normal hemostasis is the result of a set of well-
regulated processes that accomplish two important
functions
They maintain blood in a fluid, clot-free state in normal vessels
They induce a rapid & localized hemostatic plug at a site of
vascular injury
- Thrombosis is inappropriate activation of normal
hemostatic processes such as formation of a blood clot
(thrombus) in uninjured vasculature or after minor injury
Both hemostasis & thrombosis are regulated by three
components
Vascular wall
Platelets
Coagulation cascade
Whenever a vessel is ruptured or severed, hemostasis is
achieved by several mechanisms:
A. After initial injury, there is brief period of vasoconstriction,
due to reflex neurogenic vasoconstriction & local secretion
of factors such as endothelin.
B. Formation of platelet Plug - primary hemostatic plug
C. Formation blood clot as a result of blood coagulation -
secondary hemostatic plug
D. Eventual growth of fibrous tissue in to the blood clot to close
the hole in the vessel permanently
Thrombosis
- Three primary factors predispose to thrombus formation
Virchow triad
Endothelial injury
Stasis or turbulence of blood flow
Blood hypercoagulability
Endothelial injury
- It is particularly important for thrombus formation
occurring in heart or in arterial circulation
- Physical loss of endothelium will lead to exposure of
subendothelial ECM , adhesion of platelets, release of
tissue factor & local depletion of prostacyclin but
dysfunctional endothelium also may lead to thrombosis
- Eg thrombus formation following endocardial injury due
to myocardial infarction , ulcerated atherosclerotic artery
Alterations in normal blood flow
- Turbulence results in arterial & cardiac thrombosis by
causing endothelial injury or dysfunction
- Stasis is major factor in development of venous
thrombosis
Example
Aortic or arterial aneurysms cause local stasis & are favored
sites of thrombosis
Myocardial infarction results in regions of non contractile
myocardium leading to stasis in the formation of mural
thrombi
Mitral valve stenosis (eg after rheumatic heart disease) results
in left arterial dilation & location for thrombus fomation
Hyperviscosity syndrome (polycythemia vera ) cause small
vessel stasis & predispose to thrombus formation
Hypercoagulability
- It is defined as any alteration of the coagulation
pathways that predisposes to thrombosis
- The causes of hypercoagulabilty can be primary
(genetic) or secondary (acquired)
Of inherited causes of hypercoagulability , mutation in
factor V gene is one of the most common causes
- A specific factor V mutation called Leiden mutation
makes the protein resistant to protein C mediated
inactivation . In these patients recurrent deep venous
thrombosis is common
Secondary (acquired) causes
High risk for thrombosis
Prolonged bed rest or immobilization
Myocardial infarction
Atrial fibrillation
Tissue damage (surgery, fracture, burns)
Cancer
Prosthetic cardiac valves
Disseminated intravascular coagulation
Antiphospholipid antibody syndrome
Morphology of thrombi
Thrombi may develop any where in the cardiovascular
system.
Thrombi are of variable size and shape depending on
their origin and cause
A thrombus both microscopically & grossly has apparent
laminations called lines of Zahn. Lines of zahn produced
by an alternating pale layers containing platelets
admixed with some fibrin and a darker layer containing
red cells.
-The most common site of arterial thrombi in descending
order are:
Coronary arteries
Cerebral arteries
Femoral arteries
- Venous thrombi most commonly affects the veins of
lower extremities (90% of cases)
Arterial thrombi Venous thrombi

Arise at the site of endothelial injury Arise at area of stasis

Grow in a retrograde fashion, against Grow in the direction of


blood flow from its site of attachment flow towards the heart

They are usually occlusive Almost invariably occlusive

Has firm attachment Has loose attachment i.e, why


propagating tail may
Undergo fragmentation.
- Bacterial or fungal infections may cause valvular damage
of the heart as it occurring infective endocarditis lead to
the development of thrombotic mass or vegetations.
- Sterile vegetations can also develop on a non infected
valves in patients with hypercoagulable state, also called
nonbacterial thrombotic endocarditis
- Verrucous (Libman-sacks) endocarditis attributable to
elevated levels of circulating antigen-antibody complexes
typically occurring in Systemic lupus erythmatous
Fate of Thrombus
Propagation
- The thrombus may accumulate more platelets and
fibrin, propagating to cause vessel obstruction

Embolization
- Thrombi may dislodges and travel to other sites in the
vasculature
Dissolution
- Thrombi may be removed by fibrinolytic activity.
- Activation of fibrinolytic pathways can lead to rapid
shrinkage & even total lyses of recent thrombi in
contrast older thrombi undergo extensive fibrin
polymerization renders the thrombus substantially more
resistant to proteolysis and lyses is ineffectual rather it
tends to become organize
Organization and recanalization
- Organization refers to the in growth of endothelial cells,
smooth muscle cells, and fibroblasts into fibrin rich
thrombus
- Organization accompanied by the formation of
capillary channels across the thrombus, re establishing
lumen continuity to some extent. This is known as
recanalization
Clinical correlations
Thrombi are significant clinically in that:
- They cause obstruction of arteries and veins
- They are possible source of emboli
Venous Thrombosis (Phlebothrombosis)
- Venous thrombosis affects veins of the lower extremity in 90% of
cases

A) Superficial venous thrombosis


Usually occur in saphenous system particularly when there are varicosities
cause local edema, pain, and tenderness, become symptomatic but rarely
embolize
Local edema due to impaired venous drainage , predispose the involved
overlying skin to infection after slight trauma developing a condition
known as varicose ulcer
B)Deep venous thrombosis
Are more serious as they may embolize
Usually start in deep veins within the calf muscles.
Although they may cause local pain & edema, unlike
Superficial vein thrombosis, they are entirely asymptomatic in
approximately 50% of patients, since deep venous obstruction
rapidly offset or relived by collateral bypass channels.
Conditions associated with DVT
- Trauma, surgery, burns result in
a: Reduced physical activity leading to stasis
b: Injury to vessels
c: Release of procagulant substance from the tissue
- Pregnancy & puerperal state increase coagulation
factors & reduced synthesis of antithrombotics
- Malnutrition, debilitating conditions and wasting
diseases such as cancer. DVT due to these conditions
known as Marantic thrombosis
- Migrating thrombophlebitis which affects various veins
throughout the body is usually of obscure etiology, but
sometimes associated with cancer particularly
pancreatic cancer. It is also known as Trosseau
syndrome
Arterial & cardiac thrombosis
- Atherosclerosis is major initiator of thrombosis related
to abnormal vascular flow & loss of endothelial integrity
- Myocardial infarction is related to dyskinetic contraction
of the myocardium as well as damage to the adjacent
endocardium & cardiac thrombi can arise
Rheumatic heart disease may result in atrial mural
thrombi due to mitral valve stenosis followed by left
atrial dilation
In addition to obstructive features, arterial thrombi may
embolize to any tissue, but particularly common in the
brain, kidney, spleen because of their large volume of in
flow of blood .
Disseminated intravascular coagulation (DIC)
It is an acute or chronic thrombohemorrhagic disorder
occurring as a result of progressive activation of
coagulation pathway beyond physiologic set point
secondary to a variety of diseases resulting in failure of
all components of hemostasis , hence the other term for
DIC is consumption coagulopathy.
Etiology & pathogenesis
- DIC is not a primary disease but coagulopathy that
occurs in the course of variety of clinical conditions .
- It may result from pathologic activation of extrinsic
and/or intrinsic pathways of coagulation or impairment
of clot inhibiting influences
Two mechanisms that trigger DIC
Release of tissue factor or thromboplastin
Widespread injury to the endothelial cells
Major disorders associated with DIC
Acute
Obstetric complication
Placental abruption
Septic abortion
Retained dead fetus
Amniotic fluid embolism
Toxemia/ preeclampsia
Infections
Gram negative sepsis
Meningococcemia
Malaria
Burn, accidental trauma
Chronic
Neoplasms
Chronic illness
Clinical course
- The consequences of DIC are two fold.
- First, there is widespread deposition of fibrin within the
microcirculation . This may lead to ischemia of more
severely affected or more vulnerable organs &
hemolytic anemia resulting from fragmentation of red
cells as they squeeze through narrowed
microvasculature (microangiopathic hemolytic anemia)
Second , hemorrhagic diathesis may dominate the clinical
picture because of consumption of platelets & clotting
factors & increase in fibrinolysis
The onset may be fulminant as endotoxic shock,
amniotic fluid embolism, chronic in case of
carcinomatosis or retention of dead fetus.
So the clinical presentation varies with stage & severity
of the syndrome. Overall 50% of patients with DIC are
obstetric patients & about 33% of patients have
carcinomatosis.
- Clinically they may present with extensive skin & mucus
membrane bleeding and hemorrhage from multiple sites,
usually from surgical incision , vein punctures or catheter
sites.
- Respiratory symptoms such as dyspnea, cyanosis may occur.
- They may present convulsion & coma in case of CNS
bleeding or acute renal failure with oligouria, less often they
may present with acrocyanosis, pre gangrenous changes in
the digits, genitalia & nose areas where blood flow is
markedly decreased.
Circulatory failure may appear suddenly & may be
progressing.
The presentations of acute DIC, as it occur in case of
trauma or obstetric conditions, dominated by bleeding
diathesis. Where as chronic DIC ,as it occurs in cancer
patients, tends to present initially with thrombotic
complications
Laboratory manifestations include
Thrombocytopenia secondary to platelets aggregation in the
thrombus,
Schistocytes or fragmented RBCs,
Prolonged PT, PTT
Reduced fibrinogen from depleted coagulation proteins & increased
fibrin degradation product (FDP) from intense fibrinolysis.
- The cardinal manifestation of DIC which correlates most
closely with bleeding is plasma fibrinogen level, i.e. low
fibrinogen means increase tendency of bleeding.
Embolism
Definition
An embolism is a detached intravascular solid, liquid or
gaseous mass that is carried by blood to sites distant
from its point of origin.
- Thrombus is source of emboli in 99% of cases
Rare forms of emboli include fat globules & bubbles of
air, amniotic fluid, infected foreign material, bits of bone
marrow, platelets aggregates, fragment of material from
ulcerating atheromatous plaque or fragment of a tumour
- Emboli lodge in vessels too small to permit further
passage , resulting in a partial or complete vascular
occlusion. The potential consequence of this is the
ischemic necrosis of distal tissue known as infarction
- Depending on site of origin, emboli may lodge in the
pulmonary or systemic circulations.
Pulmonary thrombembolism
In more than 95% of instance venous emboli originate from deep leg vein
thrombi.
The effect of pulmonary embolism depends on the size of the embolus and on
the state of pulmonary circulation.
A large thrombus extending up to the femoral or iliac vein may become
detached & block the out flow tract of the right ventricle, the main pulumonary
trunk, impact across the bifurcation, also called saddle embolus or both of its
branches causing sudden death by circulatory arrest, sudden death, right side
heart failure (cor pulmonale) or cardiovascular collapse occur when 60% or
more of the pulmonary circulation is obstructed with emboli.
- Most pulmonary emboli i.e around 60-80% are clinically silent because they
are very small
- Embolic obstruction of medium sized arteries manifest as
pulmonary hemorrhage but usually does not cause
infarction because dual blood inflow to the area from
bronchial circulation.
But in the presence of left side heart failure, infarction could
occur.
- A patient who has had one pulmonary embolus is at high
risk of having more.
- A person with multiple emboli over time may have right
sided heart failure
Systemic thromboembolism
Refers to emboli travelling within arterial circulation.
Most (80%) arise from intra cardiac mural thrombi, two
third of which are associated with left ventricular wall
infarcts and another quarter with dilated left atria
secondary to rheumatic valvular heart disease.
The remainder from aortic aneurysm, thrombi on
ulcerated athrosclerotic plaques or fragmentation of
valvular vegetation.
Unlike venous emboli, which tend to lodge primarily in
one vascular bed (the lung), arterial emboli can travel
to a wide variety of sites.
The major sites for arteriolar embolization are the lower
extremities (75%) & the brain (10%), with the rest in the
intestines, kidney & spleen.
Crossed embolism
Crossed or paradoxical embolism occurs in the presence
of patent foremen ovale when an embolus is transferred
from the right to the left side of the heart, then to
systemic circulation.
Fat Embolism
-Usually follows fracture of bones and other type of tissue
injury, globules of fat frequently enter the circulation.
Although traumatic fat embolisms occur usually it is
asymptomatic in most cases and fat is removed.
- Fat embolism syndrome is characterized by pulmonary
insufficiency, neurologic symptoms, anemia &
thrmbocytopenia
- The pathogenesis of fat emboli probably involves both
mechanical obstruction & biochemical injury.
- Initially micro emboli of neutral fats cause occlusion of
pulmonary or cerebral microvasculature further
exacerbated by local platelets and erythrocyte aggregation.
- In addition free fatty acid released from natural fat globules
cause local toxic injury to endothelium, platelets activation
& recruitment of leukocytes with release of free radicals &
protease, completing the vascular assault.
- Fat embolism syndrome typically being 1 to 3 days after injury
during which the raised tissue pressure caused by swelling of
damaged tissue forces fat in to marrow sinusoid & veins.
- The features of this syndrome are a sudden onset of dyspnea,
blood stained sputum, tachycardia, mental confusion with
neurologic symptoms including irritability & restlessness,
sometime progress to delirium & coma.
- Anemia & thrombocytopenia
- Diffuse petechial rash in non dependent areas in 20% to 50%
of cases
Air embolism
Gas bubbles within the circulation can obstruct vascular
flow and cause distal ischemic injury almost as readily as
thrombotic masses. Air may enter the circulation during:
Obstetric procedures
Chest wall injury
In deep see divers & under water construction workers.
Neck wounds penetrating the large veins
Cardio thoracic surgery.
Arterial catheterization & intra venous infusion.
Generally, in excesses of 100cc is required to have a
clinical effect and 300cc or more may be fatal.
The bubbles act like a physical obstructions and may
coalesce to form frothy mass sufficiently large to
occlude major vessels
Amniotic fluid embolism
It is a grave but un common, unpredictable complication of labor
which may complicate vaginal, caesarean delivery and abortions. It
had mortality rate over 80%.
- The amniotic fluid containing fetal material enters via the placental
bed, the ruptured uterine veins.
- The onset is characterized by sudden sever dyspnea, cyanosis,
hypotensive shock followed by seizure & coma of the laboring mother.
- If patient survives, the initial crisis pulmonary edema typically
develops & in 50% cases they will develop DIC due to fetal material
activation of the coagulation cascade.
The classic finding is or are the presence of:
Squamous epithelial cells in pulmonary microcirculation shed
from fetal skin.
Lanugo hair
Fat from vernix caseosa.
Infarction
Definition
- An infract is an area of ischemic necrosis caused by
occlusion of either the arterial supply or venous
drainage in a particular tissue.
Nearly 99% of all infarcts result from thrombotic or
embolic events & almost all result from arterial
occlusion. Other mechanism include
Local vasospasm
Expansion of atheroma due to hemorrage in to athermotous
plaque.
External compression of the vessels. e.g trauma
Twisting of vessels as in sigmoid volvulus or ovarian
torsion
Entrapment of vessels at hernial sacks etc.
Infarction caused by venous thrombosis are more likely
to occur in organs with single venous outflow channels,
such testis & ovary.
Factors that determine the size & development of an
infract.
A. The nature of vascular supply
The presence of dual blood supply as it occur in the lung, liver,
hand & forearm may also offset the occurrence of infarction
rapidly unlike renal & splenic circulation, which have end
arterial supply.
B. Rate of development occlusion:
Slowly developing occlusions are less likely to cause infraction
since they provide time for the development of collaterals.
C. Vulnerability or susceptibility to hypoxia
The susceptibility of a tissue to hypoxia influences the
likelihood of infarction.
Neurons undergo irreversible damage when deprived of their
blood supply for only 3 to 4 minutes.
Myocardial cells die after 20-30min of ischemia. Fibroblasts
are more resistant, especially those in the myocardium
D. Oxygen content of blood
Partial obstruction of the flow of blood in an anemic or
cyanotic patient may lead to tissue infarction.
Types of infarcts
Infarcts are classified depening on:
A. The basis of their color (reflecting the amount hemorrhages)
1. Hemorrhagic (red)
2. White(anemic)
B. The presence or absence of microbial infection
1. Septic
2. Bland
A.Red infarcts
.It occurs
1) Venous occlusions as in ovarian torsion
2) In loose tissues such as lung which allow blood to collect in
infarcts zone.
3) Tissues with dual circulations (eg. lung), permitting flow of blood
from unobstructed vessel in to necrotic zone.
4) In tissues that were previously congested because of sluggish out
flow.
5) When flow is re established to a site of previous arterial occlusion
& necrosis
B. White infarcts
- It occurs in arterial occlusion or in solid organs such as
heart, spleen, kidney, where the solidity of the tissue
limits the amount of hemorrhage that can percolate or
seep in to the area of ischemic necrosis from the nearby
capillaries.
Morphology
Gross
- All infarcts tend to be wedge shaped, with the occluded vessel at
the apex and the periphery of the organ forming the base.
- In the days following infarction, the products of the dead cells
diffuse out & promote an acute inflammatory reaction at the
margin, narrow rim of hyperemia and edema, so that the infracted
site become better defined.
- Following inflammation, some of them may show recovery,
however, most are ultimately replaced with scars except the brain
Microscopy
- The dominant histologic feature of infarction is ischemic
coagulative necrosis. The brain is an exception to this
generalization, where liquifactive necrosis is common
Shock
- A state in which the failure of the circulatory system to
maintain adequate cellular perfusion resulting in wide
Spread reduction in delivery of oxygen & nutrients to
tissues
Regardless of the underlying pathology, shock
constitutes systemic hypoperfusion owing to reduction
either in cardiac out put or in the effective circulating
blood volume.
The end results are hypotension followed by impaired
tissue perfusion and cellular hypoxia
Hypovolumic shock
Definition:
Reduction in circulating blood volume which result in
reduction in preload lead to inadequate left ventricular
filling, reflecting as a decreased in left & right ventricle
end diastolic volume and pressure, culminating in
decreased cardiac output
Causes of hypovolumic shock include hemorrhage, fluid
loss from burns ,diarrhea & vomiting
Cardiogenic shock
- It results from myocardial pump failure (severe depression of
cardiac performance).
Causes
Myopathic
a) Acute myocardial infraction i.e. usually occur
if 40% left ventricle mass & more on the right ventricle is involved by infarction
b) Mycocarditis
c) Dilated cardiomyopathy/hypertrophic cardiomyopathy
d) Myocardial depression in septic shock
Mechanical
I. Intra cardiac
a) Left ventricle outflow obstruction eg. Aortic stenosis,
hypertrophic cardiomyopathy
b) Reduction in forward cardiac out put e.g. Aortic
regurgitation, MR
c) Arrhythmia.
II.Extra cardiac
.It is an obstructive shock
a) Pericardial tamponade (gross fluid accumulation in the
pericardial space) results in a decreased ventricular diastolic
filling CO
b) Tension pneumothorax (gas accumulation in pleural space)
Decrease venous return by creating a positive pressure.
c) Acute massive pulumonary embolism. Occupying 50-60% of
pulumonary vascular bed.
d) Severe pulmonary hypertension
Distributive shock
Definition:
- Refers to a group of shock sub types caused by
profound peripheral vasodilatation despite normal or
high cardiac output
Cause:
Septic shock
Anaphylactic shock
Neurogenic shock
Septic shock
Sepsis
Definition: is a systemic response to severe infection
mediated via macrophage-derived cytokines that target
end organ receptors in response to infection or SIRS
that has suspected or proven microbial etiology.
Septic shock
Definition: a kind of shock caused by systemic microbial
infection, most commonly by gram negative infection
(end toxic shock ) but can also occur with gram positive
or fungal infections.
Or
Sepsis with
1.Hypotension, arterial blood pressure less than 90mmHg
or 40mmHg less than the patients normal BP
2.Organ dysfunction
3.Unresponsive to fluid administration
Pathogenesis of septic shock:
- It has a mortality rate of over 50% ranking the first
among causes of death in intensive care unit
- It results from spread & expansion of an initially
localized infections like pneumonia in to the blood
stream.
- Most causes of septic shock (~70%) caused by
endotoxin producing gram-negative bacilli, hence the
term endotoxic shock .Endotoxins are bacterial wall
lipopolyschardes (LPS) released when cell walls are
degraded.
- LPS consists a core of toxic fatty acid (lipid A) & a
complex polysaccharide coat unique to each bacterial
species. Analogues molecules in the walls of gram-
positive bacteria & fungi can also elicit septic shock.
LPS bind with CD14 molecule on leucocytes, especially
monocytes & macrophages, endothelial cells &others.
Depending on the dosage of LPS protein complex,
initiation of a cascade of cytokine mediated events take
place
The mononuclear phagocytes respond to LPS by
producing TNF which in turn induces IL 1 synthesis.
TNF & IL-1 both act on endothelial cells to produce
further cytokines like IL-6, IL-8 & secondary effectors
like NO & PAF (platelet aggregating factor). .
Generally high levels of all of the above result in:
Systemic vasodilation
Diminished myocardial contractility
Wide spread endothelial injury & activation, alveolar capillary
damage Adult respiratory distress syndrome
Activation of the coagulation system result in DIC.
Neurogenic shock
- Shock may occur in setting of anesthetic accident or
spinal cord injury due to loss of vascular tone &
peripheral pooling of blood
Anaphylactic shock
- It is initiated by a generalized Ig-E mediated
hypersensitivity response , is associated with systemic
vasodilation & increased vascular permeability.
Stages of shock
Uncorrected shock passes through 3 important stages:
1) An initial non progressive phase
- It is also called a period of early compensatory period,
during which compensatory mechanisms are activated
& perfusion of vital organs maintained.
Mechanisms
i. A variety of neurohumoral mechanisms operate:
A decrease in cardiac out put will stimulate peripheral & central
baroreceptors with subsequent intense sympatho adrenal stimulation.
The net effect is
tachycardia, HR CO
peripheral vasoconstriction ABP, is a major auto compensatory response.
renal conservation of fluid
ii) The fall in renal perfusion stimulate the renin aldosterone secretion
mechanism.
2. Progressive stage
- Characterized by tissue hypoperfusion with onset of worsening
circulatory & metabolic imbalances including acidosis.
- There is a wide spread tissue hypoxia.
- Anaerobic glycolysis result in excessive lactic acid production.
The lactic acid reduces tissue PH & blunts vasomotor
response. Anoxic injury to endothelial cells result in DIC.
- Clinically , the patient may become confused & the urine
output declines
3. An irreversible stage
- A stage at which, even if hemodynamic disorders are corrected,
survival is not possible
- Widespread cell injury is caused by lysosomal enzyme leakage
- Myocardial contractile function worsens due to nitric oxide
synthesis
- If ischemic bowel allows intestinal flora to enter the circulation,
endotoxic shock may be superimposed
- At this point, the patient has complete renal shutdown due to
acute tubular necrosis
Morphology
- All organs are affected in severe shock. The cellular &
tissue change induced by shock are essentially those of
hypoxic injury so manifest as organ dysfunction. [MODS]
Heart
Focal or widespread coagulation necrosis
May manifest subendocardial necrosis
Myocardial infarction
Brain
- Its dysfunction occur when cerebral auto regulation or
compensatory mechanism fail. As cerebral & coronary
auto regulation try to maintain normal level of blood
pressure at DBP near to 50 mmHg, below which auto
regulation is lost. The brain manifest as boundary
zone[border zone] infarction.
Lung
- In established shock pulmonary function may
deteriorate rapidly due to a combination of causes:
Pulmonary edema
Alveolar collapse
Intra microvascular fibrin and leucocytes accumulation as
result of infection. Infection causes inflammation with
exudation of protein (fibrin) to alveolar space. These features
collectively known as shock lung or adult respiratory distress
syndrome (ARDS)
Kidney
- Exhibits extensive tubular ischemic injury, i.e. acute
tubular necrosis. Manifested as oligouria, anuria &
electrolyte disturbance.
Clinical course of shock
Patient may manifest with a weak and rapid pulse,
tachypenia & cool, clammy, cyanotic skin. In septic
shock, skin initially be warm & flushed because of
peripheral vasodilation. The patient may present with
confusion, restlessness, decrease in urine out put, coma
and death.
- The prognosis varies with the origin of shock & its
duration.80-90% of young patients with hypovolumic
shock survive where as cardiogenic shock & septic
shock carry mortality rate up to 75%
Thank you

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