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Clinical Medicine II > Pulmonary Embolism > Flashcards

Pulmonary Embolism Flashcards

1
Q

what is the 3rd leading cause of death amongst hospitalized patients?

A

pulmonary embolism

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2
Q

what is a pulmonary embolism?

A

Obstruction of the pulmonary artery or one of its branches due to embolism that travels from elsewhere in the body

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3
Q

what is the most common cause of PE?

A

Thrombus (VTE) – MOST COMMON

-usually starts as DVT in lower leg

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4
Q

what is VTE?

A

venous thromboembolism

  • One of three major cardiovascular causes of death
  • Most common preventable cause of death among hospitalized patients
  • Medicare no long reimburses hospital for DVT/PE occurring after hip or knee replacement surgery
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5
Q

what is virchow’s triad?

A

Everything that puts you at risk for developing VTE

  1. Alterations in blood flow (i.e. stasis)
  2. Vascular endothelial injury
  3. Alterations in the constituents of the blood (i.e. inherited or acquired hypercoagulable states)
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6
Q

what are the classifications of PE?

A

acute, subacute, chronic

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7
Q

what is acute PE?

A

signs and symptoms develop immediately after obstruction of pulmonary vessels prompting evaluation (sudden development of symptoms)

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8
Q

what is subacute PE?

A

patients present days or weeks following initial event

Didn’t have profound symptoms on first day, but slowly getting SOB and not feeling well, chest discomfort not subsiding and now the patient presents

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9
Q

what is chronic PE?

A

slowly develop symptoms of pulmonary hypertension over many years

A lot of small PEs as they accumulate over time (years) the patients will get progressively SOB and DOE and eventually it will result in pulmonary hypertension

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10
Q

what can render patients hemodynamically unstable?

A

massive or submissive PE

  • Hypotension (BP <90 mmHg for >15 min)
  • Severe right ventricular failure can lead to death from shock
  • Death occurs within first 2 hours
  • Risk of death remains elevated up to 72 hours after presentation
  • May need fibrinolytic (thrombolytic) therapy – b/c want to bust the clot
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11
Q

what BP is considered hemodynamically unstable from massive PE?

A

-Hypotension (BP <90 mmHg for >15 min)

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12
Q

what happens to the heart in massive PE?

A

Severe right ventricular failure can lead to death from shock

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13
Q

when does death occur from massive PE?

A

within first 2 hours

-Risk of death remains elevated up to 72 hours after presentation

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14
Q

what may you need for massive PE?

A

May need fibrinolytic (thrombolytic) therapy – b/c want to bust the clot

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15
Q

what are the 3 different locations of PEs?

A

<b>Saddle (3-6%) – largest ones, on both sides (R & L main arteries)</b>

  • 22% HD unstable
  • 5% mortality

Segmental – one of the branches

Subsegmental – small branch off of a branch

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16
Q

what are common risk factors for PEs?

A

Post-operative (recent surgery)- Very high risk

Sedentary state (Hospitalized/bedrest, Prolonged travel, lifestyle)

Malignancy

Hx of VTE in the past

Pregnancy - estrogen puts you at risk for VTE

> 25 cigs/day

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17
Q

what are types of inherited thrombophilia?

A

Factor V Leiden Mutation – causes resistance to activated protein C

Prothrombin Gene Mutation – increases plasma prothrombin concentration

Deficiency of proteins C and S

Antithrombin III deficiency
Anticardiolipin antibodies (antiphospholipid syndrome)
  • *Antithrombin, Protein C and Protein S are naturally occurring coagulation inhibitors
  • therefore, if have deficiencies of these then makes you hypercoagulable
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18
Q

what do you test for if pt has VTE and have no explanation for why they have it?

A

inherited thrombophilia

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19
Q

what is embolization?

A

Venous thrombi are dislodged and travel

-called PE if travels to lungs

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20
Q

where can emboli travel to?

A

lung - then called PE

to arterial system if there is a <b>patent foramen oval or atrial septal defect</b>
-goes from R side of heart to L side of heart and out to body

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21
Q

what are the symptoms of a PE?

A

-Sudden shortness of breath
<b>-Pleuritic chest discomfort – hurts when take deep breath or cough</b>
-Heart palpitations – b/c commonly have tachycardia

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22
Q

initial pt assessment - history for PE

A

<b>consider risk factors</b>

  • Recent surgery or sedentary state
  • Family history of clotting disorders (specifically ask about if someone in their family has had DVT or PE before)
  • <b>Calf cramping</b>, sudden shortness of breath, pleuritic chest pain

<b>-If patient is coming in with sx’s of PE, specifically ask about calf cramping b/c could be a DVT</b>

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23
Q

what is the wells’ criteria for PE?

A

likelihood of the pt having a PE

Criteria:
-signs &amp; six's of DVT
-alternative dx less likely than PE
<b>-HR >100/min</b>
-immobilization >3 days; surgery w/in 4 weeks
-prior PE or DVT
-hemoptysis
-cancer

wells score <2.0 - low likelihood
wells score 2-3 - mod likelihood
wells score >6 - high likelihood

24
Q

what is D-dimer?

A

Degradation product of cross-linked fibrin

<b>sensitive test</b> - most people who have VTE, will have pos D-dimer

<b>not specific</b> - elevated in states of inflammation

25
Q

when do you do D-dimer for DVT and PE?

A

Only use D-dimer testing in low probability patients when ruling out DVT and low to mod probability when ruling out PE

26
Q

do you measure D-dimer on super duper uber low low probability patients?

A

NO!!!

27
Q

what will you see on CXR for PE?

A

<b>“Hampton’s Hump Sign” – wedge shaped infarction from PE</b>

  • Rarely see CXR finding of PE
  • If patient has infarcted part of their lungs from PE then may see wedge shaped opacification
28
Q

what about multiple segmental & sub segmental pulmonary emboli? common in who?

A

-Common in patients with chronic emboli over years

29
Q

what is the most common imaging modality to dx PE?

A

CT angiography

30
Q

what are the advantages & disadvantages of using CT angiography to dx PE?

A

Advantages:

  • Readily available
  • Fast
  • Minimally invasive
  • Can detect alternative diagnosis

Disadvantages:
-Expensive
-Radiation Exposure
<b>-Contraindicated in patients with renal failure b/c of contrast dye, contrast allergies, and pregnancy</b>

31
Q

who is CT angiography contraindicated in?

A

Contraindicated in patients with renal failure b/c of contrast dye, contrast allergies, and pregnancy

32
Q

what does V/Q scan (ventilation/perfusion scan) measure?

A

Measures ventilation (air going in and out of the lungs) and perfusion (gas exchange)

<b>Ventilation/Perfusion mismatch SIGN OF PE***</b>
-Plenty of air getting into the lungs, but not air isn’t perfusing the whole lung

33
Q

what about venous lower extremity ultrasound?

A

<b>***Relies on loss of vein compressibility</b>
-Determines if positive

Occasionally thrombus can be directly visualized

34
Q

what are the EKG features of PE?

A

<b>SINUS TACHYCARDIA</b>

S1, Q3, T3 - “classic” but not sensitive or specific for PE

R ventricular strain pattern

  • T wave inversions in R & anterior precordial leads (V1-V4) +/- inferior leads (II, III, aVF)
  • <b>most specific</b>

Complete or incomplete RBBB

Non-specific ST or T waves changes (50%)

35
Q

what is the most specific feature on EKG for PE?

A

R ventricular strain pattern
-T wave inversions in R & anterior precordial leads (V1-V4) +/- inferior leads (II, III, aVF)

<b> associated w/high pulmonary pressures</b>
<b> most specific</b>
<b> sign that PE is so significant that it’s causing right ventricle dysfunction</b>

36
Q

what is the most common EKG feature associated with PE?

A

sinus tachycardia

37
Q

what can an echocardiogram in PE show & differentiate?

A

evidence of R heart strain (RV enlargement or RV dysfunction – not squeezing well)
-See dilated ventricle that is floppy – not pushing right amount of blood into the lungs that it should be whole RV is not contracting well

Can differentiate MI from PE

38
Q

what is primary treatment of venous thromboembolism?

A

Clot dissolution with thrombolysis (tPA) or removal of PE by embolectomy (reserved for high risk of adverse clinical outcome)

-For extreme cases where people are unstable or significant R heart dysfunction

39
Q

what is secondary treatment for venous thromboembolism?

A

Anticoagulation with anticoagulants or placement of inferior vena cava filter

40
Q

who are high risk patients?

A
  • Hemodynamic instability
  • RV dysfunction (hypokinesis) – pumping less
  • RV enlargement

Elevated Troponin

  • Stress on R heart can cause elevated Troponin (not an infarct)
  • If elevated then know the heart is really suffering and is bad PE
41
Q

what is the foundation for successful treatment of DVT and PE? what does the treatment do?

A

anticoagulation

-stabilizes clot, does not dissolve clot

42
Q

what is the initial treatment of VTE?

A

initial treatment is with parenteral drugs

-NEED TO GET THEM ON ANTICOAG’S IMMEDIATELY AND NEEDS TO BE THERAPEUTIC LEVEL IMMEDIATELY

43
Q

what are the parenteral drugs used for VTE?

A
  • Unfractionated heparin
  • LMWH
  • Fondaparinux
  • Rivaroxaban (Xarelto)
  • Dabigatran (Pradaxa)
  • Apixaban (Eliquis)
  • Edoxaban (Savaysa)
44
Q

which anticoagulants allow for single drug therapy, eliminating the need for initial parenteral anticoagulation?

A

Rivaroxaban and apixaban

45
Q

which anticoagulants are initiated after a short course of parenteral anticoagulation regimen?

A

Dabigatran and edoxaban

46
Q

what do clinical trials show about Rivaroxaban (Xarelto), Dabigatran (Pradaxa), Apixaban (Eliquis), Edoxaban (Savaysa)?

A

Clinical trials have shown the newer anticoagulants for VTE to be “non-inferior” to Warfarin in terms of efficacy and possibly safer in terms of bleeding risk

47
Q

what do you add with the parenteral agents for long-term anticoagulation?

A

Parental agents are continued as ‘bridge’ to stable long-term anticoagulation with Warfarin

48
Q

what anticoagulant drug should cancer pts with PE stay on long-term?

A

Cancer patients should stay on LMWH long-term – do better on parenteral drug

49
Q

what is the duration of anticoagulation for provoked clot and what are causes of provoked clots?

A

<b>Provoked clot – low rate of recurrence -> 3-6 months anticoagulation<b></b></b>

  • Post-operative
  • Trauma
  • Estrogen exposure</b></b>
50
Q

what is the duration of anticoagulation for unprovoked clot and what are causes of unprovoked clots?

A

<b>Unprovoked clot -> Indefinite anticoagulation</b>

  • Idiopathic – no explanation
  • Long haul air travel – b/c of sedentary state
  • Some hypercoagulable conditions (anticardiolipin antibodies) -> Puts you at risk for DVT
51
Q

what are the indications for IVC filters?

A

<b>IVC filters prevents clots from getting through</b>

  1. Active bleeding precludes anticoagulation (i.e. gastrointestinal hemorrhage and can’t anticoagulated them b/c of their active bleed)
  2. Recurrent venous thrombosis despite intensive anticoagulation
    - Anticoagulation failure
  3. High risk patients who are not candidates for fibrinolysis
52
Q

what are complications of IVC filters?

A

<b>Caval thrombosis causing marked bilateral leg swelling
-Filters themselves can cause clots to form on top of them</b>

Double the DVT rate

53
Q

how can you prevent VTE?

A

Use heparin or LMWH at lower dose for PPX in hospitalized patients

Warfarin is used peri-operatively by some orthopedic services

54
Q

prognosis of PE - major adverse outcomes

A

Recurrent thromboembolism

  • Once had DVT or PE, more likely to have another one
  • Rate depends on adequate anticoagulation & clinical nature (unprovoked)

Pulmonary hypertension Late outcome – end stage

Death

  • If left untreated, mortality rate is 30%
  • Most deaths attributable to PE occur during the first week following diagnosis due to recurrent VTE and shock – Reason why you don’t wait to start anticoag’s
55
Q

what is the PERC Rule?

A
  • If low risk patient for PE & don’t even think you need to order D-dimer, then do PERC rule for PE
  • If any criteria for the PERC rule are (+), then can’t r/o PE so get D-dimer

Clinical Medicine II (10 decks)

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