Pulmonary Embolism

Question 1

pulmonary embolism

Answer 1

• thrombus within arterial bed
• 30% mortality rate if a large vessel is obstructed
• high rate of recurrence

Question 2

embolism

Answer 2

blood clot (thrombus) or air/other things obstructing blood flow that mobilizes within vessels

Question 3

etiology

Answer 3

• d/t DVT
• fracture
• air
• ruptured amniotic sac

Question 4

explain the etiology of DVT

Answer 4

• thrombus within femoral, iliac, or popliteal veins
• DVT itself is often not life-threatening if the clot is not obstructing a major vein, but when it travels to vital organ circulation = major problem
• into inferior vena cava -> RA -> R ventricle -> pulm artery -> pulm capillaries -> pulm vein (clot gets caught in smaller vessel of pulm circuit)

Question 5

explain the etiology of a fracture

Answer 5

exposed marrow -> fatty bone marrow released, enters circulation and moves as an emboli, reaching the pulm circuit

Question 6

explain the etiology of ruptured amniotic sac

Answer 6

• hemorrhage -> matter from amniotic fluid can get into circulation and cause an embolus

Question 7

patho

Answer 7

i. DVT -> embolus -> r. side of heart -> pulm circulation ->
thrombus in arterial bed -> dec perfusion -> platelets
attracted to site of thrombus d/t abn in vessel

ii. platelets degranulate (to release mediators to attract
more platelets) but degranulation also causes bronchial
and pulm constriction

iii. hemodynamic instability d/t obstr and further
constriction of vessel

iv. reflexive bronchoconstriction

v. ventilation:perfusion imbalance -> hypoxemia and
systemic hypoxia

vi. dec CO (obstr in lungs -> dec blood flow into L. side of
heart = less blood to pump out into systemic circuit)

vii. l/o surfactant
- w/ impeded circulation, there’s decreased fluid to
form surfactant
- T2 alveolar cells that prod. surfactant are ischemic
and have decreased function, furthering decrease in
surfactant levels
- results in atelectasis d/t walls sticking together

viii. R. sided heart failure
- obstr in pulm circuit, which receives blood from R.
side, so r. ventricle is pumping against inc resistance
= inc workload on r. side of heart = failure

Question 8

surfactant

Answer 8

• function: decreases adhesion forces and prevents walls of alveoli from sticking together on exhalation
• composed of phospholipids, cholesterol, proteins and fluid

Question 9

manifestations

Answer 9

• based on size of vessel obstruction and severity
• dyspnea, tachypnea (compensatory), and chest pain from hypoxemia and hypoxia
• tachycardia (compensatory) d/t dec CO and hypoxia

Question 10

diagnosis

Answer 10

• Hx, Px
• ABGs
• D-dimer
• LDH3
• lung scan (131 I-HSA, IV)
• CT chest
• pulmonary angiogram (most effective but most invasive)

Question 11

LDH3

Answer 11

lactate dehydrogenase: enzyme and serum marker that measures injury to cells in the lungs

Question 12

D-dimer

Answer 12

fibrin degradation product, formed from breakdown of clot/fibrin

Question 13

lung scan (131 I-HSA, IV)

Answer 13

• non-invasive
• 131 I = radioactive isotope of iodine
• HSA = human serum albumin
• albumin is tagged with 131 I and is introduced via IV
• when it gets to the pulm circuit, it will move until it hits point of obstr

Question 14

treatment

Answer 14

• stat intervention
• maintain CP function
• thrombolytics and anticoagulants
• address cause (ie. DVT) to decrease recurrence