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Flashcards in VTE Deck (59)
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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