Dr. TARENI DAS; HAEMODYNAMIC DISORDERS.pptx

Dr. Tareni Das, Scientist, Division of Pathology, ICAR-
IVRI, Izatnagar
Dr. Tareni Das, Scientist, Division of pathology

Importance of vascular system
 Delivery of nutrients
 Removal of waste
( Appx. 60% of lean body weight is water, intracellular-
40% and extracellular(15% interstitial+ 5% plasma
water)

Circulatory system
 Blood
 Central pump- heart
 Blood distribution- arterial
 Collection- venous
 Exchange of nutrients- microcirculation ( arteriole,
metaarteriole, capillary, post capillary venule)
 ( continuous capillary-lung, brain,muscle, bone,
thymus, fenestrared capillary- villi, choroid plexus,
discontinuous capillary- liver, spleen)
 Lymphatics- draining fluid from extravascular spaces
into vascular system

Derangements of fluid balance
 Hypermia
 Congestion
 Haemorrhage
 Thrombosis
 Embolism
 infarction
 oedema
 shock

Hypermia
 Active engorgement of vascular beds with normal/
decreased outflow of blood
 Always acute
 Occurs due to increased metabolic activity of tissue in
order to supply additional nutrients/ oxygen
Acute General Hyperaemia:
Systemic disease ( pasteurellosis, eryspelas: due to rapid
heart beat)
Renal disease: increased fluid retention

.
 Acute Local Active Hyperaemia
 Most common type
 Aetiology:
 Neurogenic mechanisms: stomach/ intestine after
meal,
 lactating mammary gland
 genital tract during oestrus
 organs of locomotion such as muscles during exercise
 Inflammation
 Gross pathology: arteries engorged with oxygenated
blood, bright red colour, warm, heavy
 Difficult to detect after death

Congestion
 Passive engorgement due to
decreased outflow with a normal /
increased inflow
 Acute general congestion:
 Heart : myocardium degeneration,
necrosis and infarction
 Lung: pneumonia, pulmonary
thrombosis and embolism,
hydropericardium,
haemopericardium, or
pyopericardium, hydrothorax,
haemothorax, and pyothorax
 Euthansia: Relaxation of smooth
muscle

. Gross lesions: cyanosis- deoxygenated blood, swollen
(oedema), cooler
 Chronic General congestion: persists for long time
results in permanent alteration( atrophy, fibrosis)
 Heart: stenosis of a valvular opening- tricuspid- liver,
mitral- lung; valvular insufficiency- blood is forced
backward through the leaky valve that obstructs the
incoming flow; myocardial failure; anomalies of the
heart, constrictive lesions
 Lung: obliteration of the capillary bed; compression of
major pulmonary vessels by tumours, cysts, or
abscesses

Gross lesions
 Liver is affected in right-sided heart failure
 nutmeg liver‘
 cardiac cirrhosis

.
Lungs are affected in the left-sided heart failure
heart-failure cells
brown induration of the lung

. Acute Local congestion
vein compression due to: malposition of the viscera
and external pressure
obstruction persists- death of cell
Partial obstruction- atrophy and fibrosis
•Chronic Local congestion;
external pressure upon a vein
obstruction within a vein

.
 HYPOSTATIC CONGESTION
 Accumulation of blood in the ventral portions of the body due to the
influence of gravity.
 Observed in cardiac injury; and in recumbent, restrained, or inactive
animals
 common in organs such as the lungs that have poorly supported
capillaries
 Agonal congestion and postmortem congestion
 Pathology:
 Veins in the ventral portion of an organ are distended with blood
 Causes Pneumonia in the case of lungs, and gangrene of the intestine
 Oedema, haemorrhage, inflammation, and necrosis are the
complicating changes
 In tissue sections, the affected veins will contain erythrocytes, on it will
be a layer of leukocytes, and above this a zone of plasma
 Its location is used in medico-Iegal cases to indicate the position of the
body at the time of death

.

HAEMORRHAGE
 Extravascular loss of blood/escape of blood from a vessel
 Two types:
 (1) haemorrhage by rhexis, when there is rupture or break of a
blood vessel
 (2) haemorrhage by diapedesis, when blood leaves through an
apparently intact vascular wall
 Aetiology:
 physiological causes
 Trauma
 Bacterial disease
 viral diseases
 Parasites
 Fungal- guttural pouch mycosis
 necrosis and destruction of vessel wall
 neoplasms

.
 Toxic chemical agents: P, As, Uremia
 Type III hypersensitivity- immunocomplex
 Ehler –Danlos syndrome- developemental collagen
defect
 Increased vascular fragility
 Thrombocytopaenia- decreased production and
increased destruction
 Defective platelet function-
Bernard-soulier syndrome( GPIb),
Glanzmann thrombosthenia-GPIIb and GPIIIa,
Storage pool disease- deficient release of granule,
Chediak-higashi syndrome- defective platelet release
of ADP

NSAID- aspirin- inhibit cyclooxygenase- decrease
thromboxane production
Uremia
 Abnormalities in clotting factors (haemophilia A, von
Willebrand's disease, DIC, vit-K def)
 Passive hyperaemia

Classification of haemorrhages
 Source: The words cardiac, arterial, venous, and
capillary haemorrhages indicate the source of blood
 Size and shape: Petechial haemorrhages-1-2 mm
 Purpura-3-5 mm
 Ecchymotic haemorrhages-1 to 2 cm
 Haematoma or haematocyst- enclosed in a tissue
cavity
 Suffusions- Diffuse, flat, irregular areas
 Extravasations- large areas
 Linear haemorrhages- crest of the fold in intestine
 Agonal haemorrhages-Petechiae or ecchymoses
associated with death struggle

.
 Location wise:
 Perivascular, perirenal, subserous, subcutaneous,
parenchymatous, subcapsular
 Haemothorax, haemopericardium,
haemoperitoneum, haemometra and haemarthrosis
 Epitasis , haemoptysis, haematemesis , enterorrhagia,
metrorrhagia , haematuria, melena, haematocele
haemosalpinx and apoplexy
 Microscopically:
 RBCs outside BV- Fresh hemorrhage- RBCs intact
 Then degraded- phagocytosed by macrophages-
Hb(red blue colour)-bilirubin( blue green colour)-
haemosiderin (Golden brown colour) detected by
Prussian blue reaction

Significance
 Hypovolemic shock when loss is >20%.
 Haemorrhage into brain, pericardial sac and
respiratory tract-very serious and may be fatal

Thrombosis
 Characterized by formation of in appropriate
thrombus of fibrin and/or platelets along with other
blood elements on the wall of blood/ lymphatic vessel,
heart.
 Thrombosis is, basically, a pathological extension of
the normal haemostatic mechanism, and depends on
three components: (i) the vascular wall, (ii) platelets,
and (iii) the blood clotting system

Endothelium
 Anti thrombotic properties
 Inhibition of platelet aggregation: Prostacyclin (PGI2)
and Nitric oxide (NO)
 Binding and inhibition of thrombin: Heparin-like
molecules and Thrombomodulin
 Fibrinolysis: Tissue plasminogen activator (t-PA)
 Prothrombotic Properties
 Favour platelet adhesion and aggregation: von
Willebrand factor
 Favour coagulation:Inhibitors of Plasminogen
activators

Platelets
 Platelet activation occurs in contact with ECM
especially collagen:
 (1) Adhesion and shape change,


. (2) Secretion (release reaction)
 Alpha granules contain fibrinogen, fibronectin,
platelet factor 4 (an antiheparin), factor V and VIII,
platelet-derived growth factor (PDGF), transforming
growth factor alpha(TGF-alpha), and P-selectin.
 Dense bodies contain adenine nucleotides (ADP and
 ATP), ionized calcium (Ca++ ions), histamine,
serotonin, and epinephrine
 (3) Aggregation: ADP, thromboxane A2

Coagulation system

Aetiology of thrombosis
(1)Endothelialinjury;
mechanical forces,
 Parasites: strongyle larvae
 Bacteria:Erysipelothrix,Stre
ptococcus,andCorynebacter
ium
 Virus: swine fever
 Arteriosclerotic lesions and
tumours
(2) Alterations in normal
blood flow: stasis and
turbulence

 (3) Blood hyper coagulability:
Increased levels of fibrinogen, prothrombin and
factors VIIa, VIlla, and Xa.
 Increased numbers (or stickiness) of platelets
 Decreased levels of inhibitors such as antithrombin
Ill, protein C, and fibrinolysins
 ( Injury, burns, suppuration, cancer, late pregnancy
and delivery)

Pathogenesis
 Platelets recognize ·the sites of endothelial injury and adhere to
the exposed subendothelial collagen and activated.
 Platelets secrete granule products (e.g., ADP) and synthesize
thromboxane
 Platelets also expose phospholipids complexes important in the
activation of intrinsic coagulation pathway,
 Tissue factor released from injured or activated endothelial cells
activates extrinsic coagulation pathway,
 ADP released from platelets stimulates formation of a reversible
primary haemostatic plug of aggregated platelets,
 Soon the primary plug is converted into a larger irreversible
secondary plug by ADP, thrombin, and TXA2
 Deposition of fibrin (derived from platelets and plasma
fibrinogen) within and around the aggregated platelets stabilizes
the mass (thrombus) and attaches it firmly to site of origin.

.
 Location of thrombi: arch of the aorta, bifurcation of a
vessel, valves- turbulence, vein- stasis

Samavati and Uhal, 2020

Classification
 Cardiac thrombi:
Valvular (Streptococcus pyogenes or Erysipelothrix
rhusiopathiae. Corynebacterium pyogenes in cattle and
Streptococcus equi in horses)
Mural: left auricle(Clostridium chauvoei)
 Arterial thrombi: Strongylus vulgaris
 Venous thrombi:
Human: leg vein
Animals: nasal vascular sinuses of the cow and horse,
the veins of the broad ligament of the cow, and in the
scrotal plexus of the horse.
 Capillary thrombi
 Lymphatic thrombi

. Mural thrombi
 Valvular thrombi
 Lateral thrombi
 Occluding thrombi
 Saddle thrombi
 Canalized thrombi
 Septic thrombi
 Parasitic thrombi
 Aseptic thrombi
 pale or white thrombus
 red thrombus
 laminated thrombus

Fate of the Thrombus
 Propagation
 Emboli formation
 Abscessation
 Dissolution
 Organization
 Calcification
.

Significance
 Emboli
 Infarction
 Oedema
 Aneurysm

.
 Difference between venous and arterial thrombi and
PM clot??/

DIC
 Extremely large number of fibrin thrombi within the
small blood vessels, including capillaries and sinusoids
 Humans: sepsis, obstetric complications, malignancy,
and major trauma
 Animals: severe systemic infections, septic (endotoxic)
shock, neoplastic diseases, extensive trauma or bums,
and following extensive surgery, swine fever, ICH, and
BT, Sarcocystosis
 Consumption coagulopathy

Embolism
 An embolus (plural emboli) is any foreign body
floating in the blood.
 Intravascular solid, liquid, or gaseous mass
Location of emboli: artery or a capillary
 Domestic animals- arteries, humans- venous
embolism, pulmonary embolism- common
 Paradoxical embolism-congenital inter-auricular or
interventricular defect

Aetiology
 Thrombi
 Bacteria
 Parasites: Dirofilaria(Pulm.
Artery), Schistosome spp, strongyle,
hook worm, ascarid, trypanosoma
spp
 Neoplasms
 Fibrin
 Fat emboli- human, G. pig,
chicken-soft fat
 Clumps of normal body
cells- amniotic fluid
 Air or gas emboli-Caisson
disease
 Broken needles
 Hair introduced in
venipuncture
 Atheromatous debris

Significance
 Large / multiple emboli- block large size / more no. of
BV
 Infection spread- septic emboli
 New tumor growth- Tumor emboli
 Infarction- heart, spleen, kidney-no collateral
circulation

INFARCTION
 An infarct is an area of ischemic necrosis caused by
occlusion of either the arterial supply, or rarely the
venous drainage in a particular tissue
 To stuff or to fill fully

Aetiology:
 Within the lumen of the vessel (Thrombi and emboli)
 In the wall of the artery (atherosclerotic plaque/ergot)
 In the periarterial tissue (expanding tumours,
abscesses, cysts, inflammatory fibrous adhesions,
ligatures and tourniquets)

Types of Infarcts
 Depends upon (1) the solidity of the organ involved
 (ii) the type of vascular occlusion
 Types:
 Pale, white or anaemic, and red or haemorrhagic
 Septic or bland

PATHOGENESIS
 Obstruction of the arterial blood supply
 Transient ischaemia- Dialation of capillary
 Engorged with blood from anatomising capillary
 Red infaracts- haemorrhagr by diapedesis( due to
hypoxic endothelial damage)
 RBCs homogenised- degeneration of the area
 Coagulative necrosis(centre to periphery)
 Zone of inflammation due to irritation
 Granulation tissue- scar tissue- distoration of organ

.
Solid organ
few haemorhage
haemolysis
Hb diffuses out/
transformed to
haemosiderin
pale infaracts
In spongy organ
more RBCs
all are not haemolysed
infaracts not become pale

FACTORS AFFECTING INFARCTION
 The nature of blood supply
 Rate of development of occlusion
 Vulnerability to hypoxaemia
 Oxygen content of blood

Appearance
 Wedge shaped
 Red infaracts- Bulged
 Pale infaracts-depressed surface
 Scar tissue- contaction and puckering of the organ

Cont…
Kidney Spleen
 pale or anaemic  Red types in animals

Cont..
Lung ( red infaracts) .
 Pig- swine fever
 cattle, sheep, and pigs -
Pasteurellamultocida

Cont..
Liver Intestine (red type)
 Clostridium haemolyticum
infection in cattle
 Migrating strongyle larvae
in horse of anterior
mesenteric artery

Heart
 Rare in animals- pale/ red
 Common in human- due to atherosclerosis

Significance
Depends upon location and size
 Death of tissue
 Organization
 Shock
 Death of the individual

Edema
 It is the accumulation of excess interstitial fluid due to
changes in distribution of fluid between interstitium
and plasma.
 Oedema fluid/ transudate- non inflammatory with
low protein and low sp. Gravity(1.012).

Formation of tissue fluid

Causes of edema
1. Increased vascular permeability
 CAUSE
 Vascular leakage associated with inflammation
Viruses(influenza, arteri virus, canine adeno virus)
Bacteria(Clostridia, E. coli, Eryspelas )
Rickettsia( Cowdria, Ehrlichia, Rickettsia)
• Neovascularization
• Anaphylaxis
• Type-III hypersensitivity
• Toxin-endotoxin, paraquat
• Clotting abnormality-DIC

MECHANISM
 In inflammation and immunological stimuli-
Histamine, bradykinin, leukotriene, substance –p:
cause endothelial contraction and increased inter
endothelial gaps
 IL-1, TNF, INF-γ: Endothelial cell retraction due to
cytoskeletal arrangement- increased inter endothelial
gaps

2. Increased intravascular hydrostatic pressure
 Portal hypertension (right side heart failure, hepatic
fibrosis
 Pulmonary hyper tension (left side heart failure, high
altutude disease)
 Local congestion
 Iatrogenic fluid overload

MECHANISM
 (45 mm Hg- 30 mm of Hg)- (30 mm of Hg-20 mm Hg)
 =15 mm of Hg-10 mm Hg
 = 5 mm Hg
 As most cause of congestion is impaied cardiac
function- cardiac oedema

Decreased intravascular osmotic pressure
 Cause
 Decreased albumin production- severe hepatic disease
malnutrition- nutritional odema
• Excessive albumin loss- protein loosing enteropathy
• Parasitic oedema- haemonchus, trichostrongyle
• Renal disease- protein loosing enteropathy- renal
oedema
• Severe burn
• Water intoxication

MECHANISM
 (45-20) mm Hg- (20-15) mm Hg
 =(25-5) mm Hg
 =20 mm Hg
 This type of edema is severe

Lymphatic obstruction
 Cause
 Lymphatic obstruction/ compression- inflammatory/
neoplastic mass, filaria, Demodex
 Congenital lymphatic aplasia/ hypoplasia
 Lympangitis- paraTB, Sporotrichosis, Epizootic
lymphangitis

MECHANISM
 (45-25) mm Hg- (25-15) mm Hg
 =(20-10) mm Hg
 =10 mm Hg

Gross change
 Swollen, increased in weight, cold
 Colour less than normal
 No pain
 Fullness and turgidity of affected area
 Doughy
 Pits on pressure
 fibrosis

Microscopic lesion
 Space-enlarged between adjacent cells
 Pink fluid
 Atrophy
 Fibrosis

Significance
 Brain, lung- oedema fatal
 S/C tissue oedema- impair wound healing

Shock
 It is a circulatory dyshomeostasis associated with loss of
circulatory blood volume, reduced cardiac output and
inappropriate peripheral vascular resistance.
 Cause :
 Severe haemorrhage
 Diarrhoea
 Burns
 Tissue trauma
 Endotoxemia
 Extensive myocardial infarction
 Massive pulmonary embolism
 Cold, exhaustion, depression,
 General anaesthesia

Types
 Cardiogenic
 Hypovolemic
 Blood maldistribution-a. Septic shock
b. Anaphylactic shock
c. Neurogenic shock

CARDIOGENIC SHOCK
 Cardiac shock results from myocardial pump failure.
CAUSE:
 myocardial damage
 Haemopericardium
 Outflow obstruction (pulmonary embolism/ stenosis)
 Compensatory mechanism- sympathetic stimulation
of heart
 Unsuccessful compensation-stagnation of blood and
progressive tissue hypoperfusion

Hypovolemic shock
Hypovolaemia means abnormally decreased volume of
circulating blood in the body which leads to decreased
blood pressure and tissue hypoperfusion.
Cause:
 loss of blood or plasma volume
 caused by haemorrhage, fluid loss from extensive skin
bums,
 Exudation from large traumatic wounds, diarrhoea,
and vomiting.
Compensatory mechanism: peripheral vasoconstriction
and fluid movement into plasma and maintain blood
flow to brain, heart, kidney

Pathogenesis
 Reduced perfusion
 Cellular hypoxia
 Anaerobic glycolysis
 Metabolic lactic acidosis
 Lowering of pH in the tissues reduces the vasomotor
response
 Arterioles dilate and blood begins to pool in the
microcirculation.
 Anoxic injury to endothelium and fluid loss to tissue
 Haemo concentration
 Decreased cardiac output
 Again tissue hypoxia and cell death

Blood maldistribution
 Characterized by decreased peripheral vascular
resistance and pooling of blood in peripheral tissue
caused by vasodilation.
 Types
 Anaphylactic shock
 Neurologic shock
 Septic shock

Anaphylactic shock
 Type -1 hypersensitivity
 The interaction of inciting substance( allergens, drug,
vaccine) with IgE bound to mast cell
 Mast cell degranulation and histamine release
 Vasodilation, IVP, hypotension, tissue perfusion

Neurogenic shock
 Trauma to brain
 Electrocution
 Fear
 Emotional stress
 Autonomic discharge- peripheral vasodilation, pooling
of blood and tissue hypoperfusion

Septic shock
 Vasodilation is caused by vascular/ inflammatory
mediators
 Cause
 LPS
 Peptidoglycan
 Lipoteichoic Acid

PATHOGENESIS
 Free LPS attaches to a circulating LPS binding protein,
CD4 and TLR4.
 LPS prevent synthesis of anticoagulants( TFPI and
thrombomodulin) from Endothelial cell
 Induce release of IL-1, TNF, IL-6, IL-8 from monocytes
and macrophages
 activate complements- C3a, C5a
 Activate XII and related intrinsic coagulation system,
 This response increases the local acute inflammatory
response and improves clearance of the infection at
low conc. of LPS

Cont..
 Higher concentration of LPS induce more IL-1, TNF and
other cytokine and induced fever, increased acute-phase
reactants
 TF expression and extrinsic coagulation system activated
 Increased expression of endothelial leukocyte adhesion
molecule
 IL-1 induce more PAF release and TPAI which causes
platelet aggregation, thrombosis, IVP
 production of nitric oxide, PGI2 increased
 Vasodilation
 Neutrophil activation and adhesion to endothelium also
increased
 which finally leads to decreased cardiac output, low
peripheral resistance and DIC leading to septic shock

Stages of shock
 Non progressive
 Neurohumoral mechanisms maintain cardiac output and
blood pressure
 Net effect is tachycardia (rapid heart beats), peripheral
vasoconstriction, and renal conservation of fluid
 Left atrial volume receptor and hypothalamic
osmoreceptor-regulate BP through ADH activation and
renin-angiotensin-aldosterone system
 ADH and Angiotensin-II cause vasoconstriction
 Decresed blood pressure in shock also causes increased
movement of fluid from interstitium to plasma to increase
plasma volume

Cont…
 Progressive stage
 If underlying causes are not corrected shock passes to
the 'progressive phase' during which there is
widespread tissue hypoxia
 anaerobic glycolysis
 Metabolic lactic acidosis
 Increased adenosine, K, increased co2, local hypoxia-
vasodilation and pooling of blood
 endothelial cells at risk of developing anoxic injury
with subsequent DIC
 The stage is characterised by tachypnoea and oliguria

Cont…
 Irreversible stage
 Multiple organ failure due to ischaemic (hypoxic) cell
death

Clinical signs
 Depressed, lethargic
 Body temperature is subnormal and skin cold
 Fall in blood pressure
 Tachycardia
 Weak pulse
 Hyperventillation
 Oligouria

LESIONS
 Acute general passive hyperaemia: Diffuse cyanotic colour
of organs with oedema, haemorrhage, thrombosis
 Heart - subepicardial and subendocardial haemorrhages
and necrosis, myofibril coagulation due to extensive
contraction of sarcomere
 Brain- cerebral oedema, ischaemia of neuron
 Kidneys - acute tubular necrosis
 Lung- pulmonary congestion, oedema, haemorrhage,
necrosis, fibrin exudation and hyaline membrane
formation
 Liver-passive congestion and centrilobular necrosis
 Intestine- congestion, necrosis, haemorrhage, oedema
 Adrenal : early phase intense yellow, later due to
exhaustion- yellow color lost

Significance
 May reverse
 Death occurs if the blood volume cannot be restored

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