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RESPIRATORY > PULMONARY EMBOLISM > Flashcards

PULMONARY EMBOLISM Flashcards

1
Q

What is DVT?

A

The formation of a thrombus in a deep vein (typically lower limbs but can be upper limbs, cerebral veins and splanchnic veins)

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2
Q

What is a PE?

A

A condition where one or more emboli usually arising from a thrombus formed in veins, are lodged in and obstruct the pulmonary arterial system causing severe respiratory dysfunction

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3
Q

What is a provoked PE?

A

associated with an antecedent (within 3 months) and transient risk factor, such as significant immobility, surgery, trauma, pregnancy or puerperium, and the use of the combined contraceptive pill or hormone replacement therapy. These risk factors can be removed, thereby reducing the risk of recurrence.

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4
Q

What is an unprovoked PE?

A

occurs in the absence of a transient risk factor. The person may have no identifiable risk factor or a risk factor that is persistent and not easily correctable (such as active cancer or thrombophilia). Because these risk factors cannot be removed, the person is at an increased risk of recurrence.

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5
Q

What is venous thromboembolism?

A

Encompasses a DVT and a PE

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6
Q

Whats the top 3 most common CVD?

A
  1. MI
  2. Stroke
  3. venous thromboembolism
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7
Q

Whats the pathophysiology behind a PE?

A

PE -> lung tissue is ventilated but not perfused -> intra-pulmonary dead space -> impaired gas exchange
The area of lung that is no longer perfused by pulmonary artery may infarct but often does not because O2 continues to be supplied bu the bronchial circulation and airways. This leads to a reduction in the cross-sectional area of the pulmonary arterial bed -> increased pulmonary arterial pressure -> reduced CO -> after several hours alveolar collapse occurs -> worsens hypoxaemia

Large or multiple emboli can abruptly increase pulmonary arterial pressure to a level of afterload that cannot be matched by the right ventricle. Sudden death may occur, or the person may present with hypotension or syncope, which might progress to shock or death due to acute right ventricular failure.

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8
Q

What are sources of emboli for a PE?

A

Thromboses e.g. DVT
Tumours
Fat
Sepsis
Foreign bodies
Air

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9
Q

Which tumours most commonly cause emboli?

A

Prostate and breast

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10
Q

What can cause a fat emboli?

A

Long-bone fractures

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11
Q

What are risk factors for PE?

A

DVT
Previous VTE
Active cancer
Recent surgery
Significant immbolitity
Lower limb fracture/trauma
Pregnancy - 6 weeks postpartum

Others: >60, COCP, HRT, obesity, medical comorbidities, long distance sedentary travel, varicose veins, superficial venous thrombosis, known thrombophilia

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12
Q

What proportion of people with a symptomatic PE will have a concomitant DVT?

A

Up to 80%

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13
Q

What proportion of those with a PE will have a recurrence within 10 years?

A

30%

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14
Q

Whats the risk of VTE if you have cancer?

A

4 x higher

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15
Q

What are complications of a PE?

A

Recurrent PE
death
Pleural effusion
Chronic thromboembolic pulmonary hypertension

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16
Q

What is chronic thromboembolic pulmonary hypertension?

A

Elevated pulmonary arterial pressure caused by chronic thromboembolism’s which obstruct blood flow through the lungs
It’s a rare and progressive form of pulmonary hypertension

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17
Q

Whats the prognosis of a PE?

A

If left untreated prognosis is poor and risk of death is high
Following treatment there may be recurrence

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18
Q

What are symptoms of a PE?

A

Dyspnoea
Tachypnoea
Pleuritic chest pain
Features of DVT
Cough and haemoptysis
Dizziness/syncope (due to right ventricular failure)

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19
Q

What are examination findings for PE?

A

Typically chest will be clear but it may present with tachypnoea, pleural rub, crackles, tachycardia and fever

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20
Q

What proportion of patients with a PE will present with the textbook triad of pleuritic chest pain, dyspnoea and haemoptysis?

A

Around 10%

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21
Q

What CXR findings may be present in PE?

A

Atelectasis
Pleural effusion
Elevation of hemidiaphragm

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22
Q

What ECG findings may be present in PE?

A

Sinus tachycardia
Non specific ST segment and T wave abnormalities
RAD
RBBB
T wave inversion in leads V1-V3
P pulmonary
S1Q3T3 (S wave in lead 1, Q wave in lead 3 and T wave inversion in lead 3)

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23
Q

What should you do if you suspect a PE?

A

Use two-level PE wells score to estimate the clinical probability of a PE
If they score more than 4 points PE is likely so arrange CTPA and if this cannot be carried out immediately offer interim therapeutic antcoagulation. If CTPA is positive then PE is diagnosed. If negative then consider proximal leg vein USS if DVT is suspected
If 4 points of less PE is unlikely so offer a D-dimer test with the result available within 4 hours. If not available offer interim therapeutic anticoagulation. If test is positive arrange CTPA. If test is negative stop interim therapeutic anticoagulation ans consider alternative diagnosis

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24
Q

What should be offered as interim therapeutic anticoag if required?

A

Apixaban or rivaroxaban (if not suitable then LMWH)

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25
Q

What secondary care investigations may be done for a suspected PE?

A

CTPA
D-diner
ABG
CXR and ECG (mainly to exclude alternative diagnosis)
Lower limb compression venous USS
Ventilation-perfusion or perfusion scintigraphy
Echocardiography

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26
Q

What are the criteria of the 2-level PE wells test?

A

Clinical signs and symptoms of a DVT - + 3 points
HR >100 - +1.5 points
Immobilisation for >3 days or surgery in past 4 weeks - +1.5 points
Previous DVT or PE - +1.5 points
Haemoptyriss - +1 point
Cancer - +1 point
Alternative diagnosis less likely than PE - +3 points

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27
Q

What are advantages of CTPA compared to V/Q scan?

A

speed, easier to perform out-of-hours, a reduced need for further imaging and the possibility of providing an alternative diagnosis if PE is excluded

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28
Q

When might you use V/Q scanning instead of CTPA?

A

If there is renal impairment i.e. you can’t use contrast, contrast allergy

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29
Q

Whats the sensitivity and specificity of D-dimer?

A

Sensitivity is up to 98%
Specificity is about 40%

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30
Q

What is VTE prophylaxis?

A

Low molecular weight heparin e.g. enoxaparin
Anti-embolic compression stockings (unless contraindicated e.g. peripheral arterial disease)

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31
Q

How is a ventilation-perfusion scan done?

A

Radioactive isotopes are inhaled to fill the lungs and a picture is taken to demonstrate ventilation
A contrast containing isotopes is injected and a picture is taken to demonstrate perfusion
The two pictures are then compared (an area of lung tissue which is ventilated but not perfused suggests a PE)

32
Q

What ABG findings might you get from a PE?

A

Respiratory alkalosis - high RR causes them to blow off extra CO2 so blood becomes alkalosis
(Different to hyperventilation syndrome as will have low pO2)

33
Q

What is a ‘massive’ PE?

A

When the PE causes haemodynamic instability (doesnt refer to the size of the clot but a larger clot is more likely to present with haemodynamic instability)

34
Q

How do we classify PE based on location?

A

Segmental and subsegemntal (lower order pulmonary vessels)
Lobar (right or left main pulmonary arteries)
Saddle (embolus lodged at the bifurcation of the pulmonary arteries)

35
Q

Whats the theory for development of VTE?

A

Virchow’s triad - venous stasis, endothelial injury and hypercoagulbale state

36
Q

What is D-dimer?

A

A fibrin-degradation product which is created when blood clots are broken down - a marker of VTE

37
Q

How do you manage a confirmed PE?

A

Supportive management - admission to hospital, oxygen, analgesia
Apixaban or rivaroxaban (LMWH if contraindicated)
Switching to long term anticoagulation - warfarin, NOAC, LMWH
If there’s a massive PE with haemodynamic compromise use thrombolysis e.g. streptokinase, alteplase or urokinase

38
Q

What validated risk stratification tool can determine the suitability of outpatient treatment of a PE?

A

Pulmonary EMbolism Severity Index score (PESI)

39
Q

What anticoagulant treatment is used first line for a PE?

A

Apixaban and rivaroxaban (both DOACs)

40
Q

What anticoagulant should you use for managing a PE if neither apixaban or rivaroxaban are suitable?

A

LMWH followed by dabigatran or edoxaban
OR
LMWH followed by a vitamin K antagonist e.g. warfarin

41
Q

What anticoagulation should you use for managing a PE in a patient with active cancer?

A

DOAC unless contraindicated

42
Q

What anticoagulation should you use for managing a PE in a patient with severe renal impairment?

A

LMWH, unfractionated heparin or LMWG followed by a vitamin K antagonist

43
Q

What anticoagulation should you use for managing a PE in a patient with antiphospholipid syndrome?

A

LMWH followed by a vitamin K antagonist

44
Q

How long should patients be anticaogulated for following a PE?

A

3 months
If unprovoked then 6 months

45
Q

How are pts with massive PEs managed?

A

Thrombolysis

46
Q

How should you manage a pt with recurrent PEs despite adequate anticoagulation?

A

Consider IVC filters - stop blood clots formed in deep veins of legs moving to pulmonary arteries (?weak evidence base)

47
Q

What are the 2 ways thrombolysis can be performed?

A

IV using a peripheral cannula
Catheter-directed thrombolysis - Directly into the pulmonary arteries using a central catheter via the right side of the heart

48
Q

What are prophylaxis measures for VTE?

A

Anti-embolism stockings or intermittent pneumatic compression
LMWH or fondaparinux

49
Q

What are examples of vitamin K antagonists?

A

warfarin sodium - drug of choice
Acenocoumarol
Phenindione

50
Q

If an immediate anticoagulation effect is required what can you give concomitantly with warfarin?

A

Unfractionated or low molecular weight heparin (warfarin can take several days to become effective as there are clotting factors already present in the bloodstream with a long half life)

51
Q

Whats the target INR for treatment of DVT or PE/

A

2.5

52
Q

Whats the main adverse effect of oral anticoagulants?

A

Haemorrhage

53
Q

What are examples of DOACs?

A

apixaban, dabigatran etexilate, edoxaban, and rivaroxaban

54
Q

Whats the moa of dabigatran?

A

reversible inhibitor of free thrombin, fibrin-bound thrombin, and thrombin-induced platelet aggregation.

55
Q

Whats the moa of Apixaban, edoxaban and rivaroxaban?

A

reversible inhibitors of activated factor X (factor Xa) which prevents thrombin generation and thrombus development.

56
Q

Whats the reversal agent licensed for dabigatran?

A

Idarucizumab

57
Q

Whats the reversal agent licensed for Apixaban and rivaroxaban?

A

Andexanet alfa

58
Q

How should you monitor someone taking warfarin?

A

Measure INR daily until within therapeutic range then twice weekly for 1-2 weeks and then weekly until at least 2 INR measurements are within therapeutic range
Then measure at long intervals e.g. every 12 weeks but decide this length dependant on stability of INR

59
Q

What are examples of parenteral anticoagulation?

A

Unfractionated heparin
LMWH
Fondaparinux
Direct thrombin inhibitors e.g. bivalirudin

60
Q

Whats the moa of fondaparinux?

A

Activates antithrombin III which potentiates the inhibition of coagulation factors Xa

61
Q

Why is unfractionated heparin used for those at high risk of bleeding compared to LMWH?

A

Because its effect can be terminated rapidly by stopping the infusion due to the shorter duration of action

62
Q

What are examples of low molecular weight heparins?

A

Dalteparin sodium
Enoxaparin sodium
Tinzaparin sodium

63
Q

Why are LMWH better for prevention of VTE compared to unfractionated heparin?

A

Just as effective and lower risk of heparin-induced thrombocytopenia

64
Q

What are the 2 types of heparin?

A

Unfractionated (standard)
LWMH

65
Q

Whats the moa of heparin?

A

Heparins generally act by activating antithrombin III. Unfractionated heparin forms a complex which inhibits thrombin, factors Xa, IXa, XIa and XIIa. LMWH however only increases the action of antithrombin III on factor Xa

66
Q

What are adverse effects of heparins?

A

bleeding
thrombocytopenia (more common with unfractionated)
osteoporosis and an increased risk of fractures (more common with unfractionated)
hyperkalaemia

67
Q

Whats the difference between administration of unfractionated heparin and LMWH?

A

Unfractionated - IV
LMWH - subcutaneous

68
Q

Whats the difference in duration of action between unfractionated heparin and LMWH?

A

Unfractionated - short
LMWH - long

69
Q

Whats the difference in MOA between unfractionated heparin and LMWH?

A

Unfractionated - activates Antithrombin III and forms a complex that inhibits thrombin, factors Xa, IXa, Xia and XIIa

LMWH - activates antithrombin II and forms a complex that only inhibits factor Xa

70
Q

Whats the difference in monitoring between unfractionated heparin and LMWH?

A

Unfractionated - monitor APTT
LMWH - no routine monitoring required

71
Q

Which heparin is standard for managing VTE treatment and prophylaxis?

A

LMWH

72
Q

When is unfractionated heparin chosen over LMWH?

A

in situations where there is a high risk of bleeding as anticoagulation can be terminated rapidly. Also useful in renal failure

73
Q

What causes heparin-induced thrombocytopenia?

A

antibodies form against complexes of platelet factor 4 (PF4) and heparin
these antibodies bind to the PF4-heparin complexes on the platelet surface and induce platelet activation by cross-linking FcγIIA receptors
Occurs 5-10 days after treatment

Causes 50% reduction in platelets, causes thrombosis and skin allergy

74
Q

What reversal agent is used for heparin?

A

Protamine sulphate

75
Q

What blood tests should be done for a suspected/confirmed PE/

A

FBC - may be anaemic if haemoptysis
CRP - may be raised
U+E - used to assess renal function before CTPA
Clotting function - important if to be started on anticoag

RESPIRATORY (22 decks)

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