1. Hemodynamic disorders (2&3 of 3)
Ali Al Khader, M.D.
Faculty of Medicine
Al-Balqa’ Applied University

2. Thrombosis See next slide -exposed ECM -tissue factor release
-reduced production of:
-PGI2
-plasminogen activators
Thrombosis
Turbulent VS laminar flow
See next slide

3. Hypercoagulability states
More in venous thrombosis
2-15% of whites carry this mutation
The most common of genetic causes
Its allele is in 1-2% of general population
Immobilization-vascular
Injury-procoagulant release-increased hepatic synthesis of coagulation factors-reduced t-PA production
Hypercoagulability states
Also increases atherosclerosis
Procoagulant tumor products
Migratory thrombophlebitis …also called: ….
Primary VS secondary
More hepatic synthesis of coagulation factors and decreased synthesis of antithrombin III
Inherited causes of hypercoagulability should be considered in young patients (<50 years of age), even when other acquired risk factors are present
Also obesity
Also aging
Less PGI2 & more platelet aggregation

4. Morphology of thrombosis
Arterial thrombi grow in a retrograde direction from the point of attachment
Venous thrombi grow with blood flow direction
Lines of Zahn: Gross/microscopic laminations…important
Venous thrombi VS postmortem clots
Thrombi on heart valves = vegetations…infective endocarditis or other causes of endocarditis (sterile endocarditis)

5. Fate of the thrombus Propagation Embolization Dissolution
Organization and recanalization

6. Venous thrombosis (phlebothrombosis)
Mainly due to stasis or hypercoagulability

7. Disseminated intravascular coagulation
Widespread activation of thrombin
Many causes, such as obstetric complications or advanced malignancies
Widespread microscopic thrombi followed by bleeding catastrophe
= consumption coagulopathy

8. Embolism Thromboembolism…systemic or venous…discussed before
Gas embolism
Amniotic fluid embolism
Fat embolism

9. Fat embolism
Long bone fractures and soft tissue crush injuries…<10% are clinically significant
Vigorous cardiopulmonary resuscitation…mostly asymptomatic
If symptomatic:
-pulmonary insufficiency
-neurologic symptoms
-anemia
-thrombocytopenia
-diffuse petechial rash
Fatal in 10%

10. Fat embolism, mechanisms
Both mechanical obstruction and biochemical injury
Direct obstruction and platelet aggregation
Fatty acid release…endothelial injury
Granulocyte recruitment and the injury they cause

11. Amniotic fluid embolism
Uncommon
Mortality rate: 80%... the most common cause of maternal death in the developed world
85% of survivors suffer some form of permanent neurologic deficit
Sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma

12. Amniotic fluid embolism, cont’d
also may find lanugo hair, fat or mucin
If survived initial crisis:
-pulmonary edema
-DIC (50%)…thrombogenic
substances from amniotic fluid

13. Air embolism Examples: -bypass surgery…coronary artery
-neurosurgery…cerebral artery
-venous such as in obstetric surgery or chest trauma…pulmonary
-decompression sickness
The bends, chokes, and caisson disease

14. Red VS white infarcts

15. Shock
= systemic hypoperfusion of tissues

16. Other causes of shock Neurogenic…anesthesia or spinal cord injury
…loss of vessel tone
Anaphylactic shock…IgE-mediated hypersensitivity
…systemic vasodilation and increased permeability

17. Septic shock The most common cause of death in intensive care units
20% mortality rate
The most common cause: Gram (+) bacteria
Not necessary for the microbe to disseminate via blood

18. Septic shock mechanisms
Vasodilation…tissue hypoperfusion
Widespread endothelial cell activation and DIC
If no microbial cause: systemic inflammatory response syndrome
(SIRS)
…extensive trauma or burns
…pancreatitis
…diffuse ischemia

19. Septic shock mechanisms, cont’d
Innate response TNF, IL-1, ROS, lipid mediators, PAF & complement activation…etc.
The derangement in coagulation is sufficient to produce disseminated intravascular coagulation in up to half of septic patients
**The resultant hypoperfusion and ischemia will cause multiorgan
failure

20. Stages of shock Nonprogressive stage:
…reflex compensatory mechanisms are activated
…vital organ perfusion is maintained
Progressive stage:
…hypoperfusion
…onset of worsening circulatory and metabolic derangement, including acidosis
Irreversible stage:
…cellular and tissue injury is so severe
…even if the hemodynamic defects are corrected, survival is not possible

21. Thank You