L11 Pulmonary Embolism

• 1. Pulmonary embolism (63/100,00)
• 2. Pulmonary Arterial HTN (0.3/100,000)

-vast majority are pulmonary embolism

-material larger than the pulmonary capillaries enters the systemic venous system and lodges in the lung

• 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

-third leading cause of CV mortality (after MI and stroke)

• 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

-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)

-typical lung findings are uncommon in PE (cyanosis, wheezes, rales, tachypnea)

-even heart findings are uncommon

• 1. Immediate Effects
• -V/Q abnormality
• -Pulmonary infarction
• -Hemodynamic instability

• 2. Later Consequences
• -recurrence after therapy
• -chronic changes

• 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

Occurs in areas with Q = 0

uncommon

• -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

-occurs for a range of time after PE (up to greater than 1 month)

-may be due to development of more clots later

1. Transient Risk Factors

2. Hypercoagulable State

3. Unprovoked Clots

• -knee or hip replacement
• -critical illness
• -trauma

• Treatment:
• -very low risk
• -3-6 months of therapy
• -no long-term medication

• 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

• -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

• -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

• -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

• MAJORITY:
• -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)

• -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

• 1. RV unable to maintain output
•      -dyspnea/dizziness during exertion
•      *esp during exertion (no reserve)

2. R ventricle failure

3. Death if left untreated