SM_169a: Pulmonary Embolism Flashcards

1
Q

Virchow’s triad for pulmonary embolism includes ______, ______, and ______

A

Virchow’s triad for pulmonary embolism includes venous stasis, vascular injury, and alterations in coagulation

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

Describe some risk factors for PE

A
  • Venous stasis: immobility, age > 60
  • Alterations in coagulation: hereditary thrombophilias, estrogen therapy, malignancy
  • Vascular injury: surgery, trauma, post-partum, indwelling vascular access, history of VTE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most PEs are from a ______ vein in the ______ ______ extremity

A

Most PEs arise from a deep vein in the proximal lower extremity

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

Most PEs result from _____, with risk highest at the _______

A

Most PEs result from embolized deep vein thrombosis, with embolization risk highest with the proximal deep veins

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

DVTs can become ______, ______, or ______ PEs

A

DVTs can become saddle, segmental, or sub-segmental PEs

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

Obstruction of a pulmonary artery causes ______, and hypoxemia in PE is caused primarily by ______

A

Obstruction of a pulmonary artery causes dead space, and hypoxemia in PE is caused primarily by V/Q mismatch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the impact of a PE on the respiratory system

A

In PE

  • Fundamental defect = dead space
  • Sudden increase in dead space in a ventilated patient -> think of PE
  • Hypocapnia more common than hypercapnia
  • Main mechanism of hypxemia is V/Q mismatching
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

A sudden increase in _______ in a ventilated patient should make you think of a PE

A

A sudden increase in dead space in a ventilated patient should make you think of a PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Main mechanism of hypoxemia in PE is ______

A

Main mechanism of hypoxemia in PE is V/Q mismatching

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

What are the mechanisms of CV collapse in PE?

A
  • Increased RV afterload -> RV dilation -> septal shift -> decreased LV preload -> decreased CO
  • Myocardial O2 supply/demand mismatch -> coronary perfusion decreases RV ischemia -> progressive RV dysfunction

(these can feed off each other to cause rapid decompensation)

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

What is the picture in the right showing?

A

Acute PE w/ “D” sign

(RV much bigger so septum looks like a “D” in systole - IV septal bowing and LV compression)

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

Additional diagnostic testing is ______ needed for PE

A

Additional diagnostic testing is almost always needed for PE

(almost no constellation of findings is sufficiently specific for VTE to obviate the need for additional diagnostic testing)

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

What are the signs and symptoms of PE?

A

PE

  • Symptoms: pleuritic chest pain +/- hemoptysis, isolated dyspnea, circulatory collapse
  • Signs: hypoxemia, tachypnea, tachycardia, crackles on exam
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

A normal chest x-ray in patient with significant respiratory symptoms should _____ suspicion for PE

A

A normal chest x-ray in patient with significant respiratory symptoms should raise suspicion for PE

(CXR helpful to identify alternative diagnoses)

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

What are the problems with using invasive angiography/venography to diagnose PE?

A
  • Invasive
  • Contrast
  • Poor test characteristics for small clots
  • Requires specialty expertise

(prior gold standard)

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

A negative lower extremity compression ultrasound ______ exclude diagnosis of PE

A

A negative lower extremity compression ultrasound does not exclude diagnosis of PE

17
Q

Describe the V/Q scan used for diagnosis of PE

A
  • Injection and inhalation of radiolabeled isotopes
  • Looking for mismatched V/Q defects
  • Most informative when high probability or normal
  • Especially challenging in patients with chronic lung disease
  • Avoids contrast
18
Q

Describe the pros and cons of using CT pulmonary angiography for diagnosing PE

A

Most frequent test obtained

  • Pros: fast, widely available, high diagnostic accuracy
  • Cons: radiation, contrast, less accurate for small sub-segmental thrombi
19
Q

Describe D-dimer use for diagnosis of PE

A

D-dimer

  • Measures product of fibrin degradation
  • Cutoff > 500 ng/mL is highly sensitive but poorly specific for PE - good rule-out test
20
Q

Wells score ____ means PE is likely, while ____ means PE is unlikely

A

Wells score > 4 means PE is likely, while ≤ 4 means PE is unlikely

21
Q

Describe the algorithm for PE diagnostic testing

A
  • High pre-test probability: straight to CTPA
  • Lower pre-test probability: D-dimer
    • If positive, CTPA
    • If negative, no further testing
22
Q

A 65 yo patient presents after a brief cardiac arrest. In the ED, he requires two vasoactive drugs to maintain a MAP > 65 mmHg. A CT-PE confirms a large saddle PE. What is the recommended therapy?

A

Fibrinolytic agent (e.g. alteplase)

23
Q

What is the acute treatment for most patients with PE?

A
  • Unfractionated heparin infusion w/ lab monitoring
  • LMWH (enoxaparin) subcutaneous injection w/ no lab monitoring
24
Q

What is the acute treatment of patients with a massive PE (PE + shock)?

A

Systemic fibrinolytic therapy

(higher bleeding risk including intracranial hemorrhage)

25
Q

If there is a high pre-test probability of PE, start _____ while pursuing evaluation

A

If there is a high pre-test probability of PE, start anticoagulation while pursuing evaluation

26
Q

A patient with a PE but contraindication to anticoagulation is treated with an ______

A

A patient with a PE but contraindication to anticoagulation is treated with an IVC filter

27
Q

What should be avoided in treatment of submassive PE?

A

Submassive PE is PE + RV dysfunction +/- myocardial injury/strain but not in shock

Do not treat with routine use of systemic fibrinolytic therapy

28
Q

Describe chronic therapy for PE

A
  • Vitamin K antagonist (warfarin)
    • Pro: low cost, reversible, safe in renal disease
    • Con: life-long blood monitoring
  • LMWH (enoxaparin)
    • Pro: class of choice in setting of malignancy, no lab monitoring
    • Con: not as reversible, difficult dosing in renal disease and weight extremes
  • Novel oral anticoagulants
    • Pro: no lab monitoring, recommended over VKA for VTE
    • Con: cost, limited options for reversal
29
Q

For chronic PE therapy, provoked VTE (clearly identifiable risk factor) is treated for ______

A

For chronic PE therapy, provoked VTE (clearly identifiable risk factor) is treated for 3 months

30
Q

For chronic PE therapy, unprovoked VTE (no identifiable risk factor) is treated for ______

A

For chronic PE therapy, unprovoked VTE (no identifiable risk factor) is treated for 3 months minimum

(consider indefinite therapy in patients at low or moderate risk of bleeding)

31
Q

For chronic PE therapy, VTE associated with malignancy is treated for _______

A

For chronic PE therapy, VTE associated with malignancy is treated for 3 months minimum

(consider extending therapy indefinitely if cancer remains active)