PE/DVT Flashcards
Sources of Emboli?
pelvic veins
upper extremity veins
DVT in legs (90%)
Non blod clot emboli sources?
Air Tumor Amniotic fluid Talc Fat
Virchow’s Triad
Stasis
Hypercoagulability
Endothelial injury
6 congenital causes of hypercoagulability?
Factor V Leiden mutation*** Prothrombin "G" mutation Protein C & Protein S deficiency Antithrombin III deficiency Dysfibrinogenemia Homocystinemia
9 acquired causes of hypercoagulability?
4 more important
estrogen* pregnancy (hormonal)* malignancy* nephrotic syndrome* thrombocytosis DIC HIT antiphospholipid antibody syndrome PNH
4+ DVT risk factors are associated with a confirmed DVT rate of ___%;
3 risk factors»_space; ___%
0 risk factors»_space; ___%
100
50
11
What factors determine the extent of physiologic consequences of PE?
The size of the embolus
Cardiopulmonary status/reserve
Neurohormonal substances
Compensation by the circulation (due to PE)?
How does this help?
Vasodilatation of uninvolved vasculature –>
- helps to decrease pulm vasc resistance
- improves V/Q in uninvolved areas
- improves overall oxygenation
What are the physiologic consequences of PE?
- increased pulm vasc resistance
- impaired gas exchange
- alveolar hyperventilation
- increased airway resistance (bronchoconstriction)
- decreased pulm compliance
What causes increase in pulm vasc resistance in PE?
- Vascular obstruction
2. Neurohumoral agents (serotonin, Endothelin)
What causes impaired gas exchange in PE?
- Increased alv dead space from vasc obstr (V/Q mismatch)
- Impaired carbon monoxide transfer (low DLCO) due to loss of gas exchange surface
- Right-to-left shunting (in massive PE)
What causes alveolar hyperventilation in PE?
reflex stimulation of irritant receptors
What are possible causes of decreased pulm compliance in PE?
lung edema, lung hemorrhage or loss of surfactant
Gas exchange abnormalities resulting from PE?
hypocapnia
hypoxemia
widened A-a gradient
What causes tachypnea associated with PE?
increased minute ventilation