Haemodynamic disorders.

Item no. 11
Haemodynamic disorders
Hyperemia, Congestion,
Hemorrhage and Shock
Dr. A K M Maruf Raza
Associate Professor of Pathology
JIMC

Haemodynamic disorder
 Haemodynamic literally meaning blood
movement.
 It is the study of blood circulation including
cardiac function and peripheral vascular
characteristics.

Hyperemia and Congestion
 Hyperemia and congestion both occurs due
to increased blood volumes with in a tissue.
 But they have different underlying
mechanisms and consequences.

Hyperemia:
 Hyperemia is an active process in which
arteriolar dilation leads to increased blood
flow.
 Affected tissues turn red because of
increased delivery of oxygenated blood.
 Example: Skeletal muscle during exercise,
In inflammation.

Congestion
 Congestion is the increase volume of
blood due to Impaired venous return.
 It is a passive process.
 The affected tissue is blue colour due to
accumulation of deoxygenated
hemoglobin.
 Example : Congestive Cardiac Failure, Venous
obstruction.

Nutmeg liver
 It is a condition of liver in chronic hepatic
congestion.
 Nutmeg liver is called because it resembles
the cut surface of a nutmeg.

Macroscopic picture of Nutmeg liver

Nutmeg liver
 Nutmeg liver is due to coulor difference in
between central and peripheral areas of liver
lobule. The central region becomes red
brown and surrounding peripheral areas
remain tan colored.
 The central region of the hepatic lobule
appears red brown and slightly depressed
due to loss of hepatocytes. The surrounding
areas remains uncongested tan colored due
to viable liver tissue.

Hemorrhagic Disorders
 Hemorrhagic disorders characterized by
excessive bleeding.
 Disorders associated with abnormal
bleeding is due to:
i. Defects in vessel walls.
ii. Platelet disorder.
iii. Coagulation factors disorder.

Shock
 Shock→Shokkas : Jerk suddenly.
 Shock is a condition in which there is
diminished cardiac output or reduced
effective circulating blood volume which
impairs tissue perfusion and leads to
cellular hypoxia.

Types of Shock
 Cardiogenic shock
 Hypovolemic shock
 Shock associated with systemic inflammation
 Neurogenic Shock
 Anaphylactic Shock

Types of Shock
Cardiogenic shock : Results from low cardiac
output due to myocardial pump failure.
Example:
Myocardial Infarction, Ventricular rupture,
Arrhythmia.
Hypovolemic shock : Results from low cardiac
output due to loss of blood or plasma volume
from circulation.
Example:
Massive Hemorrhage, Fluid loss in Severe
vomiting, diarrhoea.

Shock associated with systemic
inflammation
 Triggered by overwhelming microbial
infections (bacterial, fungal), burns, trauma,
pancreatitis.
 Massive accumulation of inflammatory
mediator occurs, that causes arterial
vasodilation, vascular leakage, and venous
blood pooling.

Types of Shock
Neurogenic Shock: Loss of vascular tone
and peripheral pooling of blood.
Example:
Anaesthetic accident, Spinal cord injury.
Anaphylactic Shock:
Example:
IgE mediated hypersensitivity.

Septic shock:
 Caused by some Gram positive, Gram
Negative bacteria and fungus.
 Pathogenesis is due to vasodilatation and
peripheral pooling of blood.
 Gram negative bacterial lipopolysaccharide
and Gram +ve cocci Exotoxin are central to
the pathogenesis.

Septic Shock
 LPS and other microbial product attaches to
the cell surface receptor CD14.
 LPS also binds with mammalian Toll-like
receptor protein-4 (TLR-4).

 Stimulation of Mammalian Toll-like receptor
protein-4 (TLR-4) have following effect :
1) Activate endothelial cells.
2) Down-regulate anticoagulant mechanism
3) Increase release of tissue factor.
4) Activate neutrophil and mononuclear cells
with the production of cytokine IL-1, TNF,
reactive oxygen species.

Stages of shock
 Shock is a progressive disorder. If
uncorrected shock can may lead to death.
Three stages
i. Nonprogressive phase/stage
ii. Progressive stage
iii. Irreversible stage

Initial nonprogressive phase
 In this stage, Reflex compensatory
mechanism are activated and perfusion of
vital organs are maintained.
 Baroreceptor reflexes, catecholamine
release, activation of the renin-angiotensin
axis, ADH release help to maintain cardiac
output and blood pressure.

Progressive stage:
 If the patient are not treated, tissue
hypoperfusion, circulatory and metabolic
imbalance including lactic acidosis occurs.
 These causes widespread tissue hypoxia.
 Due to widespread tissue hypoxia, vital
organs are affected and begin to fail.

Irreversible stage
 In irreversible stage the cellular and tissue
injury is so severe that even if the
hemodynamic defects are corrected survival
is not possible.

Thrombosis
The formation of a solid or semisolid mass
within the cardiovascular system from the
constituents of the blood during life is
called Thrombus.
Thrombosis is the process of formation of
thrombus within the cardiovascular system
from the constituents of the blood during
life.

Virchow Triad
 Three primary abnormalities leads to
thrombus formation (called Virchow triad):
(1) Endothelial injury.
(2) Stasis or turbulent blood flow.
(3) Hypercoagulability of the blood.

Endothelial injury
 Endothelial injury leads to platelet activation.
 Inflammation, infectious agents,
hypercholesterolemia and cigarette smoke
causes endothelial injury and promote
thrombosis.

Endothelial Injury:
 Severe endothelial injury may trigger
thrombosis by exposing vWF and tissue
factor.
 Important site for thrombus formation is in
the heart and in arterial circulation.
 Example: Thrombus formation in myocardial
Infarction, In ulcerated plaque of
atherosclerosis.

Alteration in normal blood flow
Turbulence and Stasis causes alteration in
normal blood flow.
 Turbulence contributes to arterial and
cardiac thrombosis.
 Stasis contributes to venous thrombi.

Alteration in normal blood flow
Stasis and turbulence:
 Promote endothelial activation.
 Disrupt laminar flow and bring platelets into
contact with the endothelium causing
endothelial injury.
 Prevent washout and dilution of activated
clotting factors

Hypercoagulability
 Hypercoagulability is the alteration of
coagulation pathways which predisposes to
thrombus formation.
 Hypercoagulability can be divided into
primary (genetic) and secondary (acquired)
disorders.

Hypercoagulable state:
 Primary:
i. Factor V mutation
ii. Prothrombin mutation
iii. Protein C deficiency
iv. Protein S deficiency
 Secondary:
i.Prolonged immobilization
ii.Myocardial infarction
iii.Tissue injury (Surgery, Burn)
IV.Cancer.
iii.Disseminated intravascular coagulation(DIC)

Lines of Zahn:
 Thrombi often have grossly and
microscopically apparent lamination called
lines of Zahn.
 This lamination is due to alternating pale
and darker layer.
 Pale layer is formed by platelet admixed
with fibrin and darker layer containing more
red cells.

Arterial thrombus VS Venous thrombus:
Arterial thrombus Venous thrombus
Usually begin at sites of
turbulence.
Occurs at sites of stasis.
Arterial thrombi tend to grow
retrograde from the point of
attachment.
Venous thrombi extend in the
direction of blood flow.
Arterial thrombi contain
relatively less RBC thus white
or pale thrombus.
Venous thrombus tends to
contain more red cells and
known as red, or stasis thrombi.
Arterial thrombi are usually Venous thrombi is always

Common sites of thrombosis
 The most common sites of arterial thrombus
is Coronary, Cerebral and Femoral artery.
 The most common sites of venous
thrombus occurs 90% cases in lower
extremities: Deep calf veins, Femoral,
Popliteal & Iliac veins.

Thrombosis in vein
 Phlebothrombosis : Thrombosis occuring
in vein.
 Thrombophlebitis : Formation of thrombi
in inflammed vein.

Difference between thrombus and post-mortem clot
Thrombus Post-mortem clot
Formed during life in
streaming blood.
Formed after death by
clotting of blood.
It is attached to the wall It is not attached.
Line of Zahn present No line of Zahn
Dry Moist

Fate of thrombus:
 Propagation.
 Embolization.
 Dissolution (Shrinkage and total
disappearance); it is the most common.
 Organization and Recanalization.

Importance of thrombus:
i. Thrombosis causes tissue injury by local
vascular occlusion.
ii. Thrombus can dislodge and become
Emboli. Emboli can cause distal vascular
occlusion.

Disseminated intravascular
coagulation (DIC)
 A thrombotic disorder turning into a
bleeding disorder.
 Associated with severe haemorrhagic
manifestations with organ dysfunction.

Disseminated intravascular
coagulation (DIC)
 Widespread inappropriate intravascular
deposition of fibrin with consumption of
coagulation factors and platelets
(Consumption Coagulopathy)

Causes of DIC:
 Obstetric complication:
i. Amniotic fluid embolism
ii. Eclampsia, Retained placenta
iii. Septic abortion
iv. Retained dead fetus
 Infections:
i.Gram negative septicemia.
ii.Severe falciparum malaria.
 Advanced Malignancy
 Widespread tissue damage in burn, trauma

Item: 13
Embolism and Infarction

Embolism
 Embolus: An embolus is a detached
intravascular solid, liquid or gaseous
masses that is carried by the blood from its
point of origin to a distant site.
 Embolism: Embolism is the formation of
emboli.
 The vast majority of emboli are dislodged
from thrombi (thromboembolism).

Embolism
 Embolus causes subsequent impaction in
vessels distant from its point of origin.
 Emboli causes partial or complete vascular
occlusion.
 And causes tissue dysfunction and
infarction.

Emboli may be/ Classification:
 Pulmonary embolism.
 Systemic thromboembolism.
 Fat and marrow embolism.
 Air embolism.
 Amniotic fluid embolism.

Pulmonary embolism
 The most common form of thromboembolic
disease.
 95% cases arises from deep leg veins-
popliteal, femoral, iliac vein.
 It can occlude the bifurcation of pulmonary
artery (Saddle embolus).

Pulmonary embolism
 Most emboli (60% to 80%) are clinically
silent because they are small initially.
 Emboli obstructing 60% or more can cause
sudden death, right heart failure.
 Paradoxical embolism: a venous embolus
passes through an interatrial or
interventricular defect and gaining access to
the systemic arterial circulation.

Systemic Thromboembolism
 Most systemic emboli (80%) arise from
intracardiac mural thrombi.
 Most come to obstruct the arteries of lower
extremities (75%) or the brain (10%), but
other tissues, including the intestines,
kidneys, spleen are also affected.

Fat and Marrow Embolism
 Fat globules—sometimes with associated
hematopoietic bone marrow—can be found
in the pulmonary vasculature.
 Usually found after fractures of long bones
or rarely in the setting of soft tissue trauma
and burns.

Air Embolism:
 Gas bubbles within the circulation can
coalesce to form masses that obstruct
vascular flow and cause distal ischemic
injury.
 Generally 100 cc or more is required to have
a clinical effect.
 Example: During delivery, chest injury,
coronary artery bypass surgery air can enter
into the blood vessels.

Decompression
sickness/Caisson disease
 It is a form of gas embolism occurs in
sudden decrease in atmospheric pressure
(Deep sea divers).
 When air breathed at a decrease
atmospheric pressure increased amount of
gas (Nitrogen) dissolved in the blood and in
tissue.

Decompression
 If that person ascends to surface too rapidly
then the dissolved nitrogen comes out of
the blood and tissue.
 The rapid formation of gas bubbles can
cause pain, edema, hemorrhage leading to
respiratory distress.

Decompression
 Scuba and deep sea divers, underwater
construction workers are at risk.
 Chronic form of decompression sickness is
called Caisson disease.

Amniotic fluid embolism
 It is a life threatening complication of labour
and immediate postpartum period.
 It is the fifth most common cause of
maternal mortality worldwide.
 The cause is the infusion of amniotic fluid or
fetal tissue into the maternal circulation via
tear in the placental membrane or ruptured
uterine vein.

Infarction
 Infarct : The dead tissue.
 Def.: An infarct is an area of ischemic
necrosis caused by occlusion of either the
arterial supply or the venous drainage in a
particular tissue.
 Myocardial infarction (MI), Cerebral
infarction, Pulmonary infarction are the
examples.

Causes of infarction
 Arterial thrombosis or arterial embolism
underlies the vast majority of infarctions.
 Local vasospasm.
 Hemorrhage into an atheromatous plaque.
 Torsion of a vessel (ovary, Bowel).
 Obstruction of hernial sac.

Infarcts classification
 Infarcts are classified according to color
and the presence or absence of infection.
 They are either red (hemorrhagic) or white
(anemic) and may be septic or bland.

Red infarct vs White infarct
Red infarct White infarct
Occurs in venous occlusions
(e.g., testicular torsion)
occur in arterial occlusions
Occurs in loose, spongy
tissues(e.g. lung)
Occurs in solid organs (e.g.
heart, spleen)
Occurs in tissues with dual
circulations
Occurs with single end-
arterial circulation
lung and small intestine heart, spleen and kidney

Infarcts tend to be wedge-shaped, with the
occluded vessel at the apex and the periphery of
the organ forming the base.

Haemodynamic disorders.

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