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Pulmonary Week 3 > VTE > Flashcards

VTE Flashcards

1
Q

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

A

F. Because of the products of platelet products

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2
Q

Why does hypoxia occur with VTE?

A

initially a V/Q mismatch issue

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3
Q

When should anticoagulation therapy be started if VTE is suspected?

A

before the diagnosis is confirmed.

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4
Q

S1Q3T3 is an ACUTE setting is indicative of what?

A

pulmonary embolism (chronically think PAH)

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5
Q

What is the mortality rate of diagnosed PE?

A

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

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6
Q

90% of VTE originate where?

A

deep veins in the legs

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7
Q

Talc emboli are common in which patients?

A

IVDU

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8
Q

How are air emboli prevented?

A

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

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9
Q

What is VIrchow’s triad?

A

triad for risk of clot formation

  • Stasis
  • Hypercoagulability
  • Endothelial injury
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10
Q

What things promote stasis of blood?

A
  • immobility/bed rest
  • anesthesia
  • CHF/cor pulmonale
  • central venous catheters
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11
Q

What things promote hypercoaguability(genetic)?

A
  • Factor V Leiden
  • Prothrombin G20210A
  • Protein C and S deficiency
  • Antithrombin III deficiency
  • Homocystinemia
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12
Q

What things promote hypercoaguability (acquired)?

A
  • estrogen use
  • pregnancy (estrogen use and pressure on IVC promotes stasis)
  • malignancy
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13
Q

What is a type of malignancy especially associated with DVT?

A

adenocarcinoma

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14
Q

Diseases with increased hypercoag?

A
  • *-Heparin induced thrombocytopenia
  • *-Nephrotic syndrome
  • DIC
  • Antiphospholipid syndrome
  • PNH
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15
Q

What things can cause endothelium injury?

A
  • homocystinemia
  • trauma/injury
  • malignancy
  • autoimmune
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16
Q

How does a pulmonary embolus affect gas exchange?

A

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

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17
Q

How does the V/Q mismatch manifest ton testing?

A

low DLCO

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18
Q

In PE, there is alveolar hyperventilation. Why?

A

reflex stimulation of J (irritant) receptors

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19
Q

Why is wheezing seen in PE?

A

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

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20
Q

How is compliance affected by PE?

A

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

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21
Q

How does the circulation compensate?

A

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

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22
Q

T or F. A high SaO2 rules out PE

A

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

But the A-a gradient will be increased

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23
Q

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

A

T.

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24
Q

What are the overall respiratory effects of PE?

A

Tachypnea (increased minute ventilation)

Hypoxemia (V/Q mismatch)

Shunting (in massive PE)

25
Q

What are the overall gas exchange effects of PE?

A

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

26
Q

What are the overall CV effects of PE?

A
  • tachycardia (50%)
  • systemic hypotension
  • decrease in CO
  • Pulmonary HTN and cor pulmonale (possibly infarction)
27
Q

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

A

pulmonary angiography

28
Q

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

A

Helical

29
Q

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

A

SOB (and tachypnea)

30
Q

Other common signs of PE?

A
  • dyspnea
  • pleuritic pain
  • loud P2
31
Q

Overall signs of PE?

A
  • tachycardia
  • tachypnea
  • hypocapnia
  • hypoxia
32
Q

How will a CXR show in PE?

A

Normal or no new changes (pleural effusions rarely)

33
Q

What kinds of atelectasis may be seen with PE?

A

Discoid Atelectasis

34
Q

What is a Hampton’s Hump?

A

Triangular area of pulmonary infarction on CXR (fairly rare)

35
Q

What is a Westermark’s Sign?

A

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

36
Q

What are some common EKG findings of PE?

A
  • Nonspecific ST-T abnormalities
  • Tachycardia
  • minority S1Q3T3
37
Q

How are WBC affected by PE?

A

normal or increased (modest)

38
Q

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

A

T. This is a byproduct of clot dissolution

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

39
Q

Is BNP elevated or lower in PE?

A

Elevated- release when the ventricles are stressed and expanded

40
Q

Other things that may be elevated?

A
  • Troponin
  • LDH
  • Bilirubin
41
Q

Why is PaCO2 low in PE?

A

J receptors are activated and blow off more CO2

42
Q

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

A

Infiniti

43
Q

What confirms PE?

A

High clinical suspicion + High Probability V/Q scan

44
Q

What are the pitfalls of V/Q scanning?

A
  • 15s breath hold need to complete test
  • better result if no structural disease existing
  • observer variability
45
Q

The majority of V/Q scans are read as _____

A

indeterminate

46
Q

What is the gold standard for PE diagnosis?

A

Pulmonary angiography

47
Q

Other techniques for PE diagnosis?

A
  • digital subtraction angiography

- MRI (takes time)

48
Q

T or F. Normal perfusion scan excludes PE

A

T.

49
Q

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

A

if clinical suspicion is low AND D-dimer below 500

50
Q

How does DVT manifest?

A
  • Swelling of the leg
  • Homan’s sign (50:50)
  • dilated superficial veins
51
Q

Why are superficial veins dilated in DVT?

A

collateral circulation

52
Q

How is DVT diagnosed (most practical)?

A

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

53
Q

How are DVTs prevented?

A
  • early mobilization
  • T.E.D. host stockings
  • Intermittent compression of the calf and thigh
54
Q

Drugs for Heparin presentation?

A

5000 units of Heparin SQ

55
Q

How are PEs and DVTs treated (same)?

A

trying to prevent the formation of subsequent clot formation

  • Heparin (monitor aPTT)
  • then Warfarin (monitor PT)
56
Q

What needs to be monitored if you give LMW Heparin?

A

Factor Xa

57
Q

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

A

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

58
Q

When are fat emboli common?

A

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

59
Q

Triad of fat emboli?

A
  • mental status changes
  • thrombocytopenia
  • Petechiae in the chest and neck

2-3 days after fall

Pulmonary Week 3 (18 decks)

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