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24 Cards in this Set
- Front
- Back
Main cause of pulmonary embolism.
Other causes? |
Main cause:
Venous Thrombo-Embolism (venous circuln, thrombosis, embolism) Other sources: Amniotic fluid air fat tumor |
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Virchow's Triad for Pathogenesis for Development of DCT
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Stasis
Altered Coagulation Intimal Injury |
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Causes of venous stasis.
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Paralysis (neuropathic, general anesthesia)
Immobilization Bed Rest Inactivity |
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Causes of intimal injury.
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Trauma (MVA)
Surgery |
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Causes of altered coagulation.
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Acq'd:
-Mets -Lupus anticoag Inherited: AT (antithrombin), PC (protein C), PS (protein S)deficiencies APC Resistance--found in 5% of population!! |
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What puts everyone at risk for DVT?
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Age > 40
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Main source of DVTs. Which veins specifically?
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95% of CLINICALLY SIGNIFICANT PE originate from legs.
Thrombi below popliteal vein rarely embolize; particularly superficial femoral vein. Below knee: not DVT Popliteal veins: DVT Superficial Femoral Vein: DVT Femoral Vein: DVT |
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Clinical manifestations of PE
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-Impaired gas exchange (hypoxia, hypocapnea, hypercapnea)
-Pulmonary Infarct (uncommon) -Pleural Effusion |
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Effect of PE on:
A-a gradient V/Q Cardiac Output |
Increases A-a gradient
Can cause both V/Q mismatch (bronchoconstriction and congestive atelectasis--i.e., localized pulmonary edema near PE), and shunt (intrapulmonary and intracardiac) Also decreases cardiac output |
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Pulmonary embolism _____ results in hypoxia because _________.
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PE usually results in hypoxia because of dec'd Cardiac Output and/or decreased V/Q
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Effect of PE on ventilation. How does this influence PaCO2?
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Hyperventilation; low PaCO2
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Effect of PE on dead space. How does this influence PaCO2?
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Inc'd dead space; high PaCO2
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When does hypercapnea occur in PE?
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When >2/3 pulmonary circulation occluded an dpatient is unable to increase ventilation (pulm dz, paralysis, sedation)
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DCT Diagnosis:
Signs/Symptoms |
Calf Pain/Swelling
Homan's sign: dorsiflex foot and induce pain Note: >90% ARE ASYX! |
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How can ultrasound assist in the diagnosis of DVT?
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U/S of popliteal vein/artery
Apply pressure If vein does not compress when pressure is applied, a clot is holding it open |
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Why is diagnosis of PE difficult? What symptoms are suspicious for PE?
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Syx are nonspecific and there is no easy, definitive test.
Clinical suspicion for PE: Syx: Dyspnea*** Tachypnea*** Fainting** Pleuritic Pain** Apprehension Cough Hemoptysis |
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What auscultatory finding is associated with PE?
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Rales
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When is A-a gradient present in PE?
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When patient is not healthy. A-a gradient almost ALWAYS present in unhealthy patients.
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Utility of D-Dimer assay in diagnosing PE.
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Very high NPV (~98%). Good for ruling out.
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What steps would you take in determining PE after a positive D-Dimer assay?
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V/Q scan or CT Pulmonary Angiogram; if positive-->stop
If negative but have clinical suspicion: Lower Extremity U/S If negative, stop. If positive, treat. |
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DVT Prophylaxis
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SQ Heparin
Pneumatic compression boots |
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Venous Thromboemolism Treatment:
For DVT For PE For PE + Risk Factor |
Immediate anticoag w/heparin
Heparin + Coumadin at least 5 days Extended anticoag w/coumadin: 3 mos for DVT 6 mos for PE >9 mos for PE + risk factor |
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When should thrombolytics be used in PE?
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People who are hemodynamically unstable (at high risk of dying)
Allows for more complete resolution of clot Increases risk of significant bleed systemically |
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When is an IVC filter indicated in PE?
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To prevent clot embolization in pats who can't be anticoag'd, have a large clot burden, and are at high risk of DVT.
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