L11 Pulmonary Embolism

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L11 Pulmonary Embolism
2013-02-10 20:25:23
Pulmonary II

Pulmonary II
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  1. Epidemiology of Pulmonary Vascular Disease
    • 1. Pulmonary embolism (63/100,00)
    • 2. Pulmonary Arterial HTN (0.3/100,000)

    -vast majority are pulmonary embolism
  2. Pulmonary Embolism Definition
    -material larger than the pulmonary capillaries enters the systemic venous system and lodges in the lung
  3. Types of Pulmonary Embolism
    • 1. Venous thromboembolism (DVT and PE)
    • 2. Iatrogenic (bone marrow from CPR, plastic tubing etc)
    • 3. Fat (fat embolism post trauma)
    • 4. Tissue cells (tumor emboli)
    • 5. Drugs and drug carriers (IV drug abuse)
    • 6. Micro-organisms (schistosomiasis)

    ***almost always due to DVT
  4. PE Epidemiology
    -third leading cause of CV mortality (after MI and stroke)
  5. DVT to PE Pathophysiology
    • Formation:
    • -near venous valves there is static flow
    • -ppl with propensity for clots tend to develop them here
    • -usually in the valve cusps of veins in the lower extremity
    • -clots predominantly made of fibrin and RBCs

    • Propagation:
    • -growth into a larger thrombus

    • Embolization:
    • -from the veins, through the heart into the pulmonary arteries
  6. DVT Symptoms and Signs
    -local pain from vein inflammation (unusual)

    -obstruction of blood flow in the vein leads to congestion and causes pain, especially in the muscles (more common)
  7. PE Symptoms and Signs
    -typical lung findings are uncommon in PE (cyanosis, wheezes, rales, tachypnea)

    -even heart findings are uncommon
  8. PE Pathophysiology
    • 1. Immediate Effects
    • -V/Q abnormality
    • -Pulmonary infarction
    • -Hemodynamic instability

    • 2. Later Consequences
    • -recurrence after therapy
    • -chronic changes
  9. Lung Perfusion Scintigraphy
  10. Ventilation/Perfusion abnormality in PE
    • V = 0 (shunt) --> No Change
    • V/Q < 1 --> Increases
    • V/Q = 1 --> Decreases
    • V/Q > 1 --> May increase
    • Q = 0 (dead space) --> Small increase

    Blood goes to areas of the lung that don't usually get perfused very well --> hypoxemia (ironically due to normal parts of the lung that are getting more perfusion than usual)

    Easy to treat --> O2
  11. Pulmonary Infarction in PE
    Occurs in areas with Q = 0

  12. Hemodynamic Instability
    • -big problem in PE
    • -RV has to work harder to push past the clot
    • -RHF

    • 1. RHF eventually leads to decreased CO
    • 2. Leads to a decreased pressure in the coronary arteries
    • 3. Low perfusion pressure in the coronary arteries and increased pressure in the RV leads to decreased perfusion of the R heart
    • 4. --> R heart MI
  13. Mortality from PE
    -occurs for a range of time after PE (up to greater than 1 month)

    -may be due to development of more clots later
  14. PE Recurrence after therapy: Categories
    1. Transient Risk Factors

    2. Hypercoagulable State

    3. Unprovoked Clots
  15. Transient Risk Factors
    • -knee or hip replacement
    • -critical illness
    • -trauma

    • Treatment:
    • -very low risk
    • -3-6 months of therapy
    • -no long-term medication
  16. Hypercoagulable State
    • 1. Factor Deficiencies:
    • -Protein C deficiency
    • -Protein S deficiency
    • -Antithrombin deficiency

    • Treatment:
    • -High Risk
    • -lifelong anticoagulation therapy

    • 2. Increases or Altered Function:
    • -APC resistance/ factor V Leiden
    • -prothrombin regulatory sequence mutation
    • -elevated factors: VIII, IX, XI
    • -elevated lipoprotein
    • -dysfibrinogenemia

    • Treatment:
    • -Modest Risk (ie: factor V leiden, very common in the population with low risk of recurrence)
    • -long term therapy, NOT lifelong
  17. Antiphospholipid Syndrome/Lupus Anticoagulant
    • -antibodies against a variety of antigens (including phospholipids on membranes)
    • -interferes with the regulation of clotting
    • -aPPT levels increased in the lab
    • -in vivo see uncontrolled clotting

    • Treatment:
    • -High Risk of Recurrence (anticardiolipin antibodies are a marker of increased risk)
    • -life-long therapy
  18. Unprovoked Clots
    • -clots that occur out of the blue
    • -plane rides, sitting long periods of time etc...

    • Treatment:
    • -judgement call
    • -have fairly high risk of recurrence
    • -but there is a corresponding risk of increased bleeding (very serious consequences)

    • 1/5 chance of getting another clot lifelong
    • 1% chance of getting a bleed every year
  19. Chronic Changes
    • -fibrin clots are usually broken down by normal anticoagulation processes
    • -every so often something incites scar formation (leading to chronic changes)
    • -after one year only about 80% of clot is gone
    • -can still have significant obstruction of perfusion long term

    • Treatment:
    • -plasminogen activator can make the clot go away faster but normal anticoagulation leads to about the same resolution long term
  20. PE Long Term Consequences
    • -dissolution, organization and return to normal cardiopulmonary status

    • MINORITY (Vascular Scarring):
    • -post-phlebitic syndrome (DVT -->scar in vein)
    • -chronic thromboembolic pulmonary hypertension (PE --> scar in lung)
  21. Chronic Thromboembolic Pulmonary Hypertension

    • -on histology will see lines of Zahn (alternating RBCs and fibrin)
    • -clot can develop it's own blood supply

    • Pulmonary HTN:
    • -compensation
    • -cross sectional area of pulmonary arteries decreases
    • -pulmonary artery pressure rises
    • -RVH develops to maintain flow
  22. Decompensation
    • 1. RV unable to maintain output
    •      -dyspnea/dizziness during exertion
    •      *esp during exertion (no reserve)

    2. R ventricle failure

    3. Death if left untreated