Hemodynamic disorders-

Thrombosis, Embolism
and Shock

Dr. Mehzabin Ahmed

 Thrombosis

 An intravascular mass of clotted blood formed in the circulation is

called a thrombus
 Thrombus is composed of blood constituents (Platelets, WBCs and
RBCs and fibrin)
 Fibrinolytic systems are activated to remove a thrombus once it is
formed
 Thrombosis can occur at any place in the circulatory system in
 Arteries  Heart valves
 Atheroma, aneurysm  Vegetations

 Veins  Ventricles
 Compression, changes in  Mural thrombus in MI
coagulability of blood  Atrium
 Atrial fibrillation, mitral stenosis
 Pathogenesis of
thrombus formation
Clinical effects of thrombi
 Arterial thrombi cause
Three main factors  loss of pulses distal to the thrombus,

predispose to thrombus  signs of impaired blood supply like

cold, pale, painful and eventual tissues
formation- the Virchow
death or infarction and gangrene
triad formation.
 Venous thrombosis
 Endothelial dysfunction  most commonly occurs in the leg veins
 In direct injury and  the area becomes tender, swollen and

inflammation reddened.
 Superficial as well as the deep veins of
 Change in flow pattern of the legs may be involved.
blood  Varicosity in the superficial veins
( saphenous veins) are prone for
 Hypertension, thrombosis.
aneurysms  The popliteal, femoral and iliac veins
can be involved by thrombosis.
 Change in blood  DVT is an important source of
coagulability thromboembolism to the pulmonary
The hypercoagulabilty states that predispose to deep vein
thrombosis (DVT)

 Advanced age, prolonged bed rest or immobilization- causes stasis

 Cardiac failure
 Trauma, surgery, burns- result in vessel injury and causes release
of coagulation promoting factors.
 Puerperal and postpartum states
 Disseminated cancers- due to release of procoagulant states.
 There are four main outcomes following thrombus formation:
 Propagation- enlarge and occlude blood vessel
 Organization- replaced by granulation tissue and fibrosis
 Recanalization – breakdown and form holes which allow blood to flow
through it
 Embolization- break off and the fragments travel to distant organs and
obstruct arterial supply
 DIC- disseminated intravascular
coagulation

 There is widespread formation of fibrin microthrombi

throughout the circulation due to circulating procoagulant

substances triggered by endothelial injury.

Endothelial injury Circulating procoagulant substances

Formation of fibrin microthrombi

 The thrombi occlude the microvasculature causing ischemia of

the tissues and results in multiple organ failure

 It results in consumption or use up of the coagulation factors

ultimately resulting in a bleeding disorder.

 Thrombo-Embolism

 Occlusion of a blood vessel by material traveling in the blood

is termed “embolism”. The mass is called an embolus
 Thrombo-emboli originating in
 systemic veins travel to the heart and impact in the pulmonary
arterial system
 the heart (mural/ vegetations) travel via the aorta to systemic
arterial circulation and impact in arteries leading to the brain,
kidneys, spleen, gut, lower limbs
 Pulmonary embolism

 Pulmonary thrombo-embolism is extremely

common and arise in the deep veins of the leg
 Depending on the size of the embolus it may
cause major, minor and minor recurrent
pulmonary embolism
 Other types of emboli

 Tumor emboli give rise to

metastatic tumors Gangrene of toes
due to emboli
 Fat and bone marrow from aortic
aneurysm
embolism are seen in
severe fracture trauma
 Nitrogen gas emboli form in
Caisson Disease
 Amniotic fluid embolism
may occur during child
birth
 Infarction
An infarct is an area of ischemic necrosis within a tissue or
organ, produced by occlusion of either its arterial supply or
its venous drainage
Causes:
 Thrombotic or embolic obstruction
 Extrinsic compression of a vessel
 Twisting of the vessels
 Compression of the blood supply of a loop of bowel in a
hernial sac
 Types of infarcts

Infarcts are divided into various groups on the basis of their

color and presence or absence of microbial contamination.

 Based on their color infarcts are called as

 Red or hemorrhagic infarcts- occur with venous
occlusions and are common in organs, which have loose
connective tissue and dual blood supply like lungs, liver
and Testis
 White or anemic infarcts- occur due to arterial occlusion
and are seen in solid organs like heart, spleen and kidney

 Based on microbial contamination

 Septic infarcts- presence of microbial contamination

 Infarction

 Lack of blood supply to an

organ leads to infarction
 Blockage of an artery
generally leads to
coagulative necrosis in
the organs supplied by
the blood vessel
 Blockage of veins causes
hemorrhagic infarcts
 Shock

 Shock is the result of collapse of the

circulatory system.
 The cardiac output is reduced and
enough blood does not reach the vital
organs like the brain and kidneys.
 It may be classified as
 Cardiogenic shock
 due to failure of the pump
 Hypovolemic shock
 due to loss of blood volume in severe
hemorrhage, diarrheas and vomiting
 Septic shock
 due to pooling of the blood in the systemic
circulation in gram negative infections due
to peripheral vasodilatation and decreased
venous return
Types of shock Clinical Examples Principal Mechanisms

Cardiogenic Myocardial infarction Failure of myocardial pump owing to

Ventricular rupture intrinsic myocardial damage, or obstruction
to outflow
Arrhythmia
Cardiac tamponade
Pulmonary embolism
Hypovolemic Hemorrhage Inadequate blood or plasma volume
Fluid loss
Vomiting, Diarrheas
Burns
Septic Overwhelming microbial infections Peripheral vasodilatation and pooling of
Endotoxic shock blood, endothelial activation / injury
Gram-positive septicemia Leukocyte-induced damage
Fungal sepsis Disseminated intravascular coagulation
Superantigens Activation of cytokine cascade
Neurogenic Anaesthetic accident Loss of vascular tone and increased vascular
Spinal cord injury permeability
Anaphylactic IgE- mediated hypersensitivity Systemic vasodilatation and increased
response vascular permeability
Pathogenesis of Septic Shock
( Bacterial lipopolysaccharide )

( Tumor Necrosis Factor )

( Interleukin – 1 )

( Interleukin - 6 & 8 )

( Nitric oxide, Platelet activating factor )

 Clinical Manifestations of Shock

 Hypotension
 Weak rapid pulse
 Tachypnea (rapid breathing)
 Cool, clammy, cyanotic skin
 In septic shock the skin may initially be warm and
flushed because of peripheral vasodilation