Lec 20 Pulmonary Thromboembolism Flashcards
(38 cards)
What is pulmonary thromboembolism?
movement of blood clot from systemic vein through R side of heart to pulmonary circulation
What is common source of thrombi to lung?
usually from lower extremities; rarely from arms, pelvis, R chambers of heart
What is virchow’s triad of risk factors for thrombosis?
- hypercoagulability
- damage to endothelium of vessel wall
- stasis/stagnation of blood flow
What are some hereditary risk factors for hypercoagulability?
- antithrombin deficiency
- protein C deficiency
- protein S deficiency
- factor V leiden
- prothrombin gene mutation
What are acquired risk factors for hypercoagulability?
- advanced age
- previous venous thromboembolus
- cancer
- obesity
- surgery
- immobilization –> long flight
- pregnancy
- estrogens
- having a catheter
What is factor 5 leiden?
- single base substitition –> factor Va resistant to action of protein C
het individuals have 3-5x increase risk of venous thromboembolism
What happens in prothrombin gene mutation?
G20210A mutation in untranslated region of prothrombin
het individuals have 30% increase in prothrombin and 2-3x increase risk of thromboembolism
What are sequalae of pulm embolism?
- have hemodynamic perturbations and impaired gas exchange
b/c mechanical obstruction of vessels + thrombus releases mediators
How does PE cause vasoconstriction?
thrombus releases mediators serotonin and thromboxane A2 causes vasoconstriction
What 3 factors determine the hemodynamic effects of PE?
- degree of cross sectional reduction of pulm vascular bed
- preexisting status of cardiopulm system [worse if high pulm pressure to start]
- physiologic consequences of hypoxic and neurohumorally mediated vasoconstriction
What happens if obstruction < 20%?
normal PAP and PVR b/c of recruitment and distension of pulm vessels
CO maintained
What happens if obstruction 30-40%?
increase PAP and modest increase RAP
What happens if obstruction > 50%?
compensatory mech overcome
CO begins to fall and RAP increases
What is maximum mean PAP right ventricle can generate in patient without prior cardiopulm disease?
40 mmHg
What happens to PaCO2 level in PE?
have increase dead space ventilation but also have increase in total minute ventilation
–> can get low CO2 [hypocapnia]
What are 5 mechanisms that can lead to hypoxemia?
- hypoventilation
- V/Q mismatch
- shunt
- diffusion impairment
- low PIO2
Does dead space ventilation cause hypoxemia?
nope! not on its own
How do you get hypoxemia due to decrease CO in pulm embolism?
have decrease CO –> decrease O2 delivery but your tissues still taking up the O2 and consume it –> lower O2 sat –> decrease CaO2
What are 4 mechs causing hypoxemia in pulm embolism?
- increased PVR
- decreased CO reducing the O2 in venous admixture
- loss of pulm surfactant
- bronchoconstriction
What is mech of increase PVR causing hypoxemia in PE?
- increased PVR –> causes increased perfusion to poorly ventilated areas and get V/Q mismatch + if really high PVR –> can get reverse shunt
What is mech of loss of surfactant causing hypoxemia in PE?
-loss of pulm surfactant after 24 hrs of occlusion –> atelectasis and edema
hypoxemia if partial thrombus resolution of perfusion but now have lack of ventilation = shunt
What is mech of bronchoconstriction in PE?
platelet mediators in thrombus cause vaso/bronchoconstriction
hypocapnia that occurs in PE also causes bronchoconstriction
WHat are the 3 potential sources of O2 for pulmonary parenchyma?
- airways
- pulm arteries
- bronchial arteries
What are symptoms of PE?
- acute onset dyspnea [most common]
- pleuritic chest pain
- hemoptysis
- syncope [rare]
