1) maintain blood in a fluit, clot-free state in normal vessels.

2) Induce a rapid and localized hemostatic plug at a site of vascular injury.

Rarely embolizes, leads to local congestion, swelling, pain, tenderness. Predisposes skin to infection from slight trauma and development of varicose ulcers.

1)MI>dyskinetic contraction of myocardium> stasis in the ventricle=site for mural thrombus

2)Rheumatic heart disease> mitral valve stenosis> L atrial dilation and fibrillation> stasis in the L atrium> thrombosis

1. Aneurysms> stasis> thrombus formation

2. Atherosclerosis, abnormal vascular flow> damage to endothelium>loss of endothelial integrity> thrombus formation

3. Vasculitis and trauma

1. Cardiac and Arterial Thrombosis

2. Propagates at site of formation

3. Obstructs vessel at the point of formation

4. Hypoxia and necrosis

5. MI, cerebral infarction, kidneys, spleen

1. Propogation

2. Generation of an embolus (Embolization)

3. Organization and recanalization

4. Dissolution (resolution)

1. Venous Thrombus

2. Propagates at site of formation

3. Obstructs vessel at pt of formation

4. Congestion &edema in vascular bed distal to obstruction

1. Cardiac and Arterial Thrombosis

2. Embolization

3. Artery at distant site

4. Systemic thromboembolism

5. MI, Cerebral infarction, Kidneys, Spleen

1. Venous thrombus (phlebothrombosis)

2. Embolization

3. Vein at distant site

4. Obstruction of critical vein eg pulmonary v

5. Pulmonary thromboembolism

-80% intracardial mural thrombi

-20% aortic aneurysms

-10% unknown

1. Fibrinolytic pathways-

   *Recent thrombi, rapid shrinkage or total lysis or

   *Older thrombi, extensive fibrin polymerization, resistant to lysis

2. Therapeutic implications- t-pa infusions effective for short time, pulmonary or coronary

Regulated by:

1.Vascular wall

2. Platelets

3. Coagulation cascade

Primary hemostasis:Endothelial injury > exposes thrombogenic substances in subendothelial ECM> platelets adhere to form plug

Secondary hemostasis: plug becomes clot, procoagulant fact acts w/platelet facts to activate coagulation cascade> thrombin activated

1. Endothelial injury

2. Abnormal Blood Flow

3. Hypercoagulability

All lead to thrombosis

1. Physical loss of endothelium

2. Exposure of the subendothelium collagen and other platelet activators

3. Platelet adhere to the basement membrane

4. Release of tissue factor and local depletion of prostacyclin.

5. Platelet aggregation and fibrin formation

Most common are mutations in factor V gene and prothrombin gene.

-elevated homocystein, deficience of anticoagulants (antithrombin III, protein C, protein S) present w/ venous thrombosis.

"consumption coagulopathy"

Thrombohemorrhagic disorder as secondary complication- forms microthrombi unevently, activates fibrinolytic mechanisms, present similar to hypoxia, and infarction.

Endothelial cells maintain liquid blood flow:

1. Block platelet adhesion and aggregation

2. Interferes with coagulation cascade- protein C, antithrombin III)

3. Lyse blood clots- synthesize t-PA

1.Failure of the heart as a pump to tissues

2. Failure of venous return to tissues

3. Failure of pump leading to shock

4. Failure of venous return leading to congestion and edema.

• Reduces cardiac output
• Reduces effective circulation of blood volume
• hypotension followed by impaired tissue perfusion and cellular hypoxia

Is a progressive disorder and if uncorrected leads to death

1. Nonprogressive- reflex compensatory mechanism to maintain perfusion to vital organs

2. Progressive- hypoperfusion, hypoxia, acidosis, pooling of blood, DIC

3. Irreversible- severe cell and tissue injury, lysosomal enzyme leakage, NO synthesis> decreased myocardial function, acute tubular necrosis > complete renal shutdown

1. Cardiogenic shock

2. Hypovolemic shock

3. Septic shock

4. Neurogenic shock

5. Anaphylactic shock

Inadequate blood or plasma volume

• severe hemorrhage
• extensive trauma or burns

• Systemic microbial infection, endotoxin (LPS) producing gram negative bacteria
• Localized infection in blood stream
• 25-75% mortality rate
• ranks 1st in deaths in ICU

IgE mediated hypersensitivity response

• vasodilation> vascular bed capacitance
• increase vascular permeability=hypotension> tissue hypoperfusion> cellular anoxia

• hypotension
• weak rapid pulse
• tachypnea
• cool, clammy, cyanotic skin

Skin may initially be warm and flushed (peripheral vasodilation)

Passive process from impaired outflow of blood from a tissue, systemic or local, cyanotic (deoxy Hb), edema.

1. Red- blood accumulates in tissue

2. White- occur with arterial occlusions