The document discusses pulmonary embolism (PE), which occurs when blood clots form in the veins (deep vein thrombosis or DVT) and travel to the lungs. Risk factors for PE include inherited factors like Factor V Leiden mutation that cause hypercoagulability, as well as acquired risks like older age, surgery, cancer, and oral contraceptives. PE can cause hypoxemia and other symptoms by obstructing blood flow and damaging the ventilation-perfusion ratio in the lungs. The document outlines inherited and acquired causes of hypercoagulability that predispose individuals to DVT and PE.

1. Common disease
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2.  Myocardial
infarction
 Stroke
 PE
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3. 1.
2.
3.
Where do 95% of pulmonary
thromboemboli originate?
What are the risk factors for pulmonary
thromboemboli?
What hemodynamic changes are brought
about by significant pulmonary
thromboemboli?
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4. 4.
5.
6.
What changes in ventilation/perfusion
relationships are brought about by
significant pulmonary thromboemboli?
What are the causes of hypoxemia in
pulmonary thromboembolism.
What are the clinical manifestations of
pulmonary thromboembolism?
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5.  Includes
• Pulmonary embolism (PE)
• Deep venous thrombosis (DVT)
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7.  Predispose
to VTE
• Vascular endothelial injury
• Hypercoagulability
• Venous stasis
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8.  Acquired
• Account for the majority of VTE cases
 Inherited
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9. >
60 years
• Most significant acquired risk factor for VTE
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10.  Most
significant risk factor for recurrent
VTE
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11. 1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Obesity
Malignancy
Surgery
Trauma
Pregnancy
Oral contraceptives
Postmenopausal hormone replacement
Long-haul air travel
Heparin-induced thrombocytopenia
Antiphospholipid antibody syndrome
Cigarette smoking
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12.  Factor
V Leiden mutation
 Activated protein C resistance
 Prothrombin gene mutation
 Elevated factor VIII levels
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13.  Physiological
1.
2.
3.
anticoagulants
Antithrombin
Protein C
Protein S
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14.  Synthesized
by the liver
 Converted to an active protease by
thrombin
• Protein C becomes an anticoagulant when it is
activated by thrombin.
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15.  Protein
produced by endothelial cells
• Enhances thrombin activation of protein C
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17.  Inactivates
factors V and VIII
 Stimulates the release of tPA from
endothelial cells
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18.  Enhances
anticoagulatory function of
protein C
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19.  Proteins
C and S
• Reduced blood levels
• Dysfunctional
•
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20.  Makes
factor V resistant to protein C
inhibition
 Hypercoagulable state
 Many patients with venous
thromboembolism have this defect

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