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Flashcards in VTE Deck (59):
1

T or F. Bronchospasm and wheezing are seldom a part of VTE

F. Because of the products of platelet products

2

Why does hypoxia occur with VTE?

initially a V/Q mismatch issue

3

When should anticoagulation therapy be started if VTE is suspected?

before the diagnosis is confirmed.

4

S1Q3T3 is an ACUTE setting is indicative of what?

pulmonary embolism (chronically think PAH)

5

What is the mortality rate of diagnosed PE?

Less than 10% but it bumps up to 30% if undiagnosed

6

90% of VTE originate where?

deep veins in the legs

7

Talc emboli are common in which patients?

IVDU

8

How are air emboli prevented?

lie patients flat and somewhat on side (Trendelenburg position) to prevent intrathoracic pressure from dropping to much

9

What is VIrchow's triad?

triad for risk of clot formation
-Stasis
-Hypercoagulability
-Endothelial injury

10

What things promote stasis of blood?

-immobility/bed rest
-anesthesia
-CHF/cor pulmonale
-central venous catheters

11

What things promote hypercoaguability(genetic)?

-Factor V Leiden
-Prothrombin G20210A
-Protein C and S deficiency
-Antithrombin III deficiency
-Homocystinemia

12

What things promote hypercoaguability (acquired)?

-estrogen use
-pregnancy (estrogen use and pressure on IVC promotes stasis)
-malignancy

13

What is a type of malignancy especially associated with DVT?

adenocarcinoma

14

Diseases with increased hypercoag?

**-Heparin induced thrombocytopenia
**-Nephrotic syndrome
-DIC
-Antiphospholipid syndrome
-PNH

15

What things can cause endothelium injury?

-homocystinemia
-trauma/injury
-malignancy
-autoimmune

16

How does a pulmonary embolus affect gas exchange?

there is increased alveolar dead space creating a V/Q mismatch and shunting

17

How does the V/Q mismatch manifest ton testing?

low DLCO

18

In PE, there is alveolar hyperventilation. Why?

reflex stimulation of J (irritant) receptors

19

Why is wheezing seen in PE?

there is increased airway resistance due to bronchoconstriction (increased serotonin production locally by the clot)

20

How is compliance affected by PE?

decreased due to lung edema, lung hemorrhage, or loss of surfactant

21

How does the circulation compensate?

there is vasodilation of uninvolved vasculature which helps to decrease the increase in PVR and improves V/Q relationship

22

T or F. A high SaO2 rules out PE

F. This is due to the compensatory effect in pulmonary circulation

But the A-a gradient will be increased

23

T or F. The A-a gradient is increased in pulmonary embolism

T.

24

What are the overall respiratory effects of PE?

Tachypnea (increased minute ventilation)

Hypoxemia (V/Q mismatch)

Shunting (in massive PE)

25

What are the overall gas exchange effects of PE?

-hypocapnia (low PaCO2)
-hypoxemia (low PaO2)
Wide A-a gradient

26

What are the overall CV effects of PE?

-tachycardia (50%)
-systemic hypotension
-decrease in CO
-Pulmonary HTN and cor pulmonale (possibly infarction)

27

What is the gold standard of picking of clots in the pulmonary circulation?

pulmonary angiography

28

What type of CT scan s used for ruling in/out PE?

Helical

29

What is the most common complaint form a patient with acute PE?

SOB (and tachypnea)

30

Other common signs of PE?

-dyspnea
-pleuritic pain
-loud P2

31

Overall signs of PE?

-tachycardia
-tachypnea
-hypocapnia
-hypoxia

32

How will a CXR show in PE?

Normal or no new changes (pleural effusions rarely)

33

What kinds of atelectasis may be seen with PE?

Discoid Atelectasis

34

What is a Hampton's Hump?

Triangular area of pulmonary infarction on CXR (fairly rare)

35

What is a Westermark's Sign?

Complete occlusion of the pulmonary artery with no vascular markings on CXR

36

What are some common EKG findings of PE?

-Nonspecific ST-T abnormalities
-Tachycardia
-minority S1Q3T3

37

How are WBC affected by PE?

normal or increased (modest)

38

T or F. D-dimer will be elevated in PE

T. This is a byproduct of clot dissolution

D-Dimer less than 500 suggest very low probability of PE

39

Is BNP elevated or lower in PE?

Elevated- release when the ventricles are stressed and expanded

40

Other things that may be elevated?

-Troponin
-LDH
-Bilirubin

41

Why is PaCO2 low in PE?

J receptors are activated and blow off more CO2

42

What are the results of V/Q scan of PE?

Infiniti

43

What confirms PE?

High clinical suspicion + High Probability V/Q scan

44

What are the pitfalls of V/Q scanning?

-15s breath hold need to complete test
-better result if no structural disease existing
-observer variability

45

The majority of V/Q scans are read as _____

indeterminate

46

What is the gold standard for PE diagnosis?

Pulmonary angiography

47

Other techniques for PE diagnosis?

-digital subtraction angiography
-MRI (takes time)

48

T or F. Normal perfusion scan excludes PE

T.

49

When can you rule out PE before even running any scans?

if clinical suspicion is low AND D-dimer below 500

50

How does DVT manifest?

-Swelling of the leg
-Homan's sign (50:50)
-dilated superficial veins

51

Why are superficial veins dilated in DVT?

collateral circulation

52

How is DVT diagnosed (most practical)?

Bilateral lower extremity Doppler exam (B mode ultrasonography) to demonstrate non-compressibility of the veins

53

How are DVTs prevented?

-early mobilization
-T.E.D. host stockings
-Intermittent compression of the calf and thigh

54

Drugs for Heparin presentation?

5000 units of Heparin SQ

55

How are PEs and DVTs treated (same)?

trying to prevent the formation of subsequent clot formation

-Heparin (monitor aPTT)
-then Warfarin (monitor PT)

56

What needs to be monitored if you give LMW Heparin?

Factor Xa

57

What is the most common cause of treatment failure in PE?

failure to achieve and maintain therapeutic anticoagulation int he first 24 hrs

58

When are fat emboli common?

after long bone fractures in the elderly (because marrow is now replaced by fat)

59

Triad of fat emboli?

-mental status changes
-thrombocytopenia
-Petechiae in the chest and neck

2-3 days after fall