Lecture 20: Pulmonary Thromboembolism Flashcards

1
Q

Factors leading to hypercoagulability (3 classes)

A

Hereditary risk factors, acquired risk factors (age, cancer, obesity), and triggering factors (surgery, immobilization, estrogens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe Factor V Leiden

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe prothrombin gene mutation

A

Mutation in prothrombin gene –> heterozygous are 30% increased risk of venous thromboembolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Three anticoagulant deficiencies

A

Protein C, protein S, antithrombin III deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Factors that lead to hypercoagulability (6)

A

Bone fractures, surgery, oral contraceptives (+ age, smoking), pregnancy (post-partum as well), foreign bodies (catheters), cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sequaelae of PE are due to what two categories…

A
  1. Mechanical obstruction; 2. Mediators released from thrombus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Two vasoconstrictive mediators released by thrombi

A

5-HT and thromboxane A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Three factors effecting the badness of a PE

A
  1. Degree of reduction of cross-sectional area of pulmonary vascular bed; 2. Pre-existing cardiopulmonary system; 3. Consequences of hypoxic/neurohumorally mediated vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Effects of obstruction

A

Normal or near-normal Pap and PVR because of recruitment and distension of pulmonary vessels; CO maintained

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Effects of obstruction >30% of pulmonary vasculature?

A

Increase in Pap and modest increase in RAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Effects of obstruction >50% of pulmonary vasculature…CO?

A

Cannot compensate, RAP incrases; CO drops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In a healthy patient, what is the max mean Pap RV can generate?

A

40 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gas exchange in PE: dead-space or shunt?

A

Dead-space (all V, no Q); PAO2 = air, PACO2 = 0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PE: hyper or hypocapia?

A

Hypocapnia because of increase in total minute ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Is dead-space ventilation a cause of hypoexmia?

A

NOPE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does hypoxemia occur in PE? (4)

A

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

17
Q

How long does it take to lose surfactant?

A

24 hours of total occlusion

18
Q

What causes bronchoconstriction in PE?

A

Platelet mediators and hypocapnia

19
Q

Is pulmonary infarction common?

A

No, because there are 3 sources of O2 to lungs (pulmonary arteries, bronchial arteries, airways)

20
Q

PE: symptoms

A

Acute onset dyspnea, pleuritic chest pain, hemoptysis, syncope

21
Q

PE: physical exam

A

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)

22
Q

Why could the lung exam be normal in PE?

A

It’s a VESSEL problem not a lung problem

23
Q

PE: X-ray (two named findings)

A

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

24
Q

PE: dx

A

CT pulmonary angiography

25
Q

What is a ventilation perfusion scan? Use for PE?

A

Imaging that looks at both ventilation and perfusion; if you have decreased perfusion but OK ventilation this may suggest PE

26
Q

What imaging modality ca be used to find a DVT?

A

Lower extremity ultrasound +/- compression (no compression = clot presence)

27
Q

In PE setting, what is the value of echocardiogram (2)

A

Evaluate RV size/fxn AND assess for RV/RA thrombus

28
Q

What does D-Dimer test look for? Sensitivity? Specificity?

A

Evidence of clot formation and dissolution; sensitive and negative predictive value (i.e. if test is NORMAL then you likely DO NOT have a PE); NOT specific and poor positive predictive value

29
Q

Fate of a thrombus…

A

Grow/propagate –> fibrinolysis –> organize and recanalize

30
Q

Do most people do OK with a PE?

A

Yes, improvement (~2 months) is usually sufficient to restore normal pulmonary hemodynamics, gas exchange, and exercise tolerance

31
Q

A minority of patients will develop…WHO classification?

A

Chronic thromboembolic pulmonary hypertension; WHO IV

32
Q

PE: tx (3 catgeories)

A

Anticoagulation (heparin), thrombolysis (tPA), surgery

33
Q

What is an inferior vena cava filter?

A

Device that traps thrombi from lower extremities

34
Q

When is an inferior vena cava filter indicated? What is the risk?

A
  1. Contraindicated to anticoagulant therapy; 2. Thromboembolism recurrence despite adequate anticoagulation; 3. Limited pulmonary vascular reserve; increased risk of DVT
35
Q

Does thrombolysis cause an increased bleeding risk? Therefore…

A

YES: ONLY FOR SICKEST PATIENTS