Thirty Flashcards

1
Q

What are the risk factors for PE?

A

Hip or leg fracture
Hip or Knee replacement
Malignancy
Previous DVT or PE

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

What is the cardiac pathophys in PE?

A

PE increases PVR which results in increased RV wall tension and increased RV dilatation and hypokinesis. RV dilatation and hypokinesis leads to septal deviation and decreased RV CO which leads to decreased preload which leads to systemic hypotension which could lead to decreased Coronary perfusion and can contribute to ischemia. RV wall tension leads to increased O2 demand. It can also lead to decreased coronary perfusion. Both of these contribute to myocardial ischemia and infarction.

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

What are the cardiovascular effects in the pathophys of PE?

A

Obstructive Shock

Pulmonary vasculature constriction (5-HT and TXA2)

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

What is the respiratory pathophys of PE?

A

Increased dead space, hypoxemia, decreased CO2 (tachypnea), PFO (right to left shunt), pulmonary infarction

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

What is the spectrum of presentations in PE? What are some signs and symptoms that point to PE? How can these lead to a diagnosis of PE?

A

The patient could be in shock or could be asymptomatic.

Symptoms: syncope, near syncope, lightheadedness, palpitations, chest pain, hemoptysis, cough, dyspnea, calf or thigh pain,

Signs: Tachypnea, tachycardia, crackles, decr. breath sounds,

The wells score combines signs, symptoms, and risk factors to give an overall likelihood of PE

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

How are D-dimers used in diagnosis of PE? What is BNP/how is it used in diagnosis of PE? What about troponin? What will blood gases tell you ?

A

By ELISA, a level of less than 500 ng/mL has a high negative predictive value for PE.

When Brain natriuretic peptide is elvated, it a marker of ventricular stretch

Troponin is a marker of myocyte death which might happen in RV overload.

They can show if the pt. is hypoxemic.

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

What does the ECG show in PE? How useful is it?

A

It most often will show sinus tach with non specific ST and T wave changes. It might include an S1, Q3, T3 pattern (Deep S in lead 1, Q wave in lead 3 and inverted T wave in lead 3)

It is neither specific nor sensitive for PE

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

What findings might be found on a chest radiograph in PE? What will the corresponding findings be on CT?

A

Westermark sign-Asymmetrical darkening due to lack of perfusion.

Hampton Hump-Pleural based wedge shaped opacity due to infarction.

On CT, you will see filling defects.

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

What are the pros and cons of CT angiography in diagnosing PE?

A

It allows you to view the vessels and see if they’re blocked. You can also see any other parenchymal abnormalities. You can see the relative sizes of the ventricles.

However, it requires contrast which can’t be used if a pt. has an allergy or renal dysfunction (elevated creatinine). It also requires more radiation. It can also miss subsegmental PE.

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

What is a V/Q scan? How is it useful in diagnosing PE?

A

Ventilation perfusion scan. Normal results are V/Q matching. In PE, there will be a lack of perfusion.

Pts. with a high clinical probability of PE and a high probability V/Q scan have a 95% likelihood of PE

Pts with a low clinical probability of PE and a low prob. V/Q scan had a 4% likelihood of PE

A normal V/Q scan virtually excludes the likelihood of PE

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

What is CUS? What does it show? When is it used? How is it done?

A

An ultrasound is used to visualize the deep veins of the leg. They then are compressed. If they are unable to be compressed, they have a thrombus.

This is an important test when CT angiography can’t be performed.

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

What are the goals of PE management? What are the treatment options?

A
– ↓ Mortality
– Stabilize the patient
• Improve gas exchange
• Circulatory abnormalities
– Prevent extension
– Prevent recurrence
– Perform risk stratification
• Echo, Troponin, BNP
• Anticoagulation
– Prevents recurrence (25% VS no
therapy)
– Anticoagulation decreases
mortality (30% to 3-5%)
• IVC Filter
• Fibrinolytic therapy
• Catheter-directed therapy
• Surgical embolectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is considered a massive PE? A submassive PE? A Low risk?

A

– Massive PE
• Acute PE with sustained hypotension
• SBP 1, ↑ BNP, ↑ troponin

– Low Risk
• Normal BP, normal BNP, normal troponin, normal RV:LV ratio

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

What drugs should be used in the initial treatment of PE? Continued treatment? Long term?

A

Inititally:

LMWH/UFH
Fondaparinux
Warfarin
Thrombolysis
Rivoroxaban
Continued: 
Warfarin
LMWH
Dabigatran
Rivoroxaban

Further:
Warfarin
Rivoroxaban
Dabigatran

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

What advantages does LMWH have over UFH?

A
  • LMWH
  • 1mg/kg q12º or 1.5 mg/kg once daily

• Advantage over UFH
– Convenient & fixed dosing
– Laboratory monitoring is not necessary
– Less incidence of thrombocytopenia

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

What is the goal of UFH? What is the big side effect?

A

• UFH
• Weight based regimen
– 80 units/kg bolus followed by 18 units/kg/hr infusion
– aPTT 1.5-2 x control (GOAL is to be therapeutic within 24º)
• Can cause thrombocytopenia

17
Q

What is fondaparinux? What are the advantages?

A
• Fondaparinux
• Comparison to UFH
– Convenient & fixed dosing
– Laboratory monitoring is not necessary
– Less incidence of thrombocytopenia
18
Q

What is the mechanism of action of Warfarin/VKA? What is the timeline for it? Why?

A
  • Warfarin/VKA
  • Mechanism of Action
  • Inhibit factor II, VII, IX & X
  • Inhibit protein C &S
  • Day 1/2
  • Overlap of 5 days is recommended & until INR ›2 x 24º
19
Q

What are the benefits of Rivaroxaban?

A
Rivaroxaban
• 15 mg PO BID x 21 days, and then 20 mg PO daily
• No overlap needed
• Benefits
– Fixed dose
– No laboratory monitoring
20
Q

What are the benefits of Dabigatran? How is it administered?

A
• Dabigatran
• 150 mg PO BID
• > after initial parenteral Rx
• Benefits
– Fixed dose
– No laboratory monitoring
21
Q

When is the placement of an IV filter indicated?

A

• Contraindication to
anticoagulation
• Recurrent VTE despite
adequate anticoagulation

22
Q

When is tPA indicated?

A
• Recombinant tissue plasminogen activator (tPA)
• INDICATIONS
– Massive PE
– Severe Hypoxemia
– RV dysfunction and injury
23
Q

When is catheter directed thrombectomy (tPA) indicated?

A
Acute PE with associated
hypotension
• Contraindications to
systemic thrombolysis
• Failed thrombolysis
• Shock likely to cause death
before systemic
thrombolysis can take effect
24
Q

When is surgical embolectomy indicated?

A
– Massive PE
• CI to systemic thrombolysis or
• Failed thrombolysis or
catheter-assisted
embolectomy or
• Shock that is likely to cause
death or before thrombolysis
can take effect