Lecture 20: Pulmonary Thromboembolism Flashcards
Factors leading to hypercoagulability (3 classes)
Hereditary risk factors, acquired risk factors (age, cancer, obesity), and triggering factors (surgery, immobilization, estrogens)
Describe Factor V Leiden
Most common cause of hereditary thrombophilia; factor Va becomes resistant to action of activated proctein C; heterozygous are 3-5 fold increased risk of venous thromboembolism
Describe prothrombin gene mutation
Mutation in prothrombin gene –> heterozygous are 30% increased risk of venous thromboembolism
Three anticoagulant deficiencies
Protein C, protein S, antithrombin III deficiency
Factors that lead to hypercoagulability (6)
Bone fractures, surgery, oral contraceptives (+ age, smoking), pregnancy (post-partum as well), foreign bodies (catheters), cancer
Sequaelae of PE are due to what two categories…
- Mechanical obstruction; 2. Mediators released from thrombus
Two vasoconstrictive mediators released by thrombi
5-HT and thromboxane A2
Three factors effecting the badness of a PE
- Degree of reduction of cross-sectional area of pulmonary vascular bed; 2. Pre-existing cardiopulmonary system; 3. Consequences of hypoxic/neurohumorally mediated vasoconstriction
Effects of obstruction
Normal or near-normal Pap and PVR because of recruitment and distension of pulmonary vessels; CO maintained
Effects of obstruction >30% of pulmonary vasculature?
Increase in Pap and modest increase in RAP
Effects of obstruction >50% of pulmonary vasculature…CO?
Cannot compensate, RAP incrases; CO drops
In a healthy patient, what is the max mean Pap RV can generate?
40 mm Hg
Gas exchange in PE: dead-space or shunt?
Dead-space (all V, no Q); PAO2 = air, PACO2 = 0
PE: hyper or hypocapia?
Hypocapnia because of increase in total minute ventilation
Is dead-space ventilation a cause of hypoexmia?
NOPE