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
How does hypoxemia occur in PE? (4)
Increased PVR (shunt) –> this can lead to intracardiac shunt due to increased right sided pressures; decreased CO reducing venous admixture; loss of pulmonary surfactant; bronchoconstriction
How long does it take to lose surfactant?
24 hours of total occlusion
What causes bronchoconstriction in PE?
Platelet mediators and hypocapnia
Is pulmonary infarction common?
No, because there are 3 sources of O2 to lungs (pulmonary arteries, bronchial arteries, airways)
PE: symptoms
Acute onset dyspnea, pleuritic chest pain, hemoptysis, syncope
PE: physical exam
Vital signs:
tachycardia, hypotension, tachypnea, hypoxemia; Lung:
may be normal OR rales (atelectasis, infarction), wheezing (bronchoconstriction), findings of pleural effusion; Cardiac:
RV heave, split S2, loud P2, systolic TR murmur, diastolic PR murmur, RV S3; Extremities:
tenderness, edema, cord (palpable clot within a vessel)
Why could the lung exam be normal in PE?
It’s a VESSEL problem not a lung problem
PE: X-ray (two named findings)
CAN BE COMPLETELY NORMAL; or rare findings: Hampton’s Hump (shallow wedge-shaped opacity in periphery of lung = infarction); Westmark’s sign: localized area of decreased lung vascular markings
PE: dx
CT pulmonary angiography
