Pulmonary embolism Flashcards

1
Q

Define pulmonary embolism

A

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

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

Define provoked PE

A

Associated with an antecedent (within 3 months) and transient risk factor, e.g. immobility, surgery, trauma, pregnancy or puerperium, and the use of the COCP or HRT.

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

Define unprovoked PE

A

Absence of a transient risk factor - e.g. active cancer, thrombophilia (risks can’t be removed)

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

Pulmonary embolism (PE) pathophysiology

A

Emboli(s), usually arising from a thrombus formed in the veins, lodges in and obstructs the pulmonary artery(ies).

  • -> lung tissue is ventilated but not perfused, resulting in an intra-pulmonary dead space and impaired gas exchange.
  • -> reduction in cross-sectional area of pulmonary arterial bed
  • -> elevation of pulmonary arterial pressure and reduction in cardiac output
  • -> alveolar collapse, which worsens hypoxaemia
  • -> hyperventilation and respiratory alkalosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens in a massive PE?

A

Large or multiple emboli can abruptly increase pulmonary arterial pressure to a level of afterload which 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.

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

What are the non-thrombotic sources of emboli? (6)

A
Tumours e.g. prostate and breast cancers
Fat e.g. long-bone fractures
Amniotic fluid
Sepsis e.g. endocarditis
Foreign bodies e.g. IVDU, broken medical equipment 
Air e.g. surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Virchow’s triad?

A

Hypercoagulability
Venous stasis
Vascular wall damage

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

Major risk factors for PE (7)

A
Deep vein thrombosis 
Previous VTE
Active cancer
Recent surgery 
Significant immobility e.g. bed rest, hospital admission
Lower limb trauma or fracture 
Pregnancy and postpartum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Other risk factors for PE (9)

A
>60yo
COCP or HRT
Obesity
Significant medical comorbidities e.g. heart disease
Long distance travel
Varicose veins
Superficial venous thrombosis
Known thrombophilias 
Other e.g. central vein catheter, nephrotic syndrome, chronic dialysis, myeloproliferative disorders, Behcet's
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complications of PE

A

Mortality, morbidity, and hospitalization

Chronic thromboembolic pulmonary hypertension (rare)

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

What is CTEPH?

A

Chronic thromboembolic pulmonary hypertension
Emboli replaced with fibrous tissue, leading to chronic obsutrction and increased pulmonary arterial pressure, which can lead to right heart failure

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

Symptoms of PE

A

May be asymptomatic
Sudden and severe pleuritic chest pain
Dyspnoea
Features of DVT (e.g. leg pain/swelling)
Retrosternal chest pain (due to right ventricular ischaemia)
Cough and haemoptysis
Dizziness and/or syncope (due to right ventricular failure)

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

Signs of PE

A
Tachycardia
Tachypnoea
Hypoxia
Pyrexia
Elevated JVP
Gallop rhythm, a widely split second heart sound, tricuspid regurgitant murmur
Pleural rub
Hypotension and cardiogenic shock (rare signs indicating central PE and/or a severely reduced haemodynamic reserve).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chest x-ray features in PE

A

Atelectasis, pleural effusion, or elevation of a hemidiaphragm
Wedge opacity

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

ECG features in PE

A

Sinus tachycardia
Non-specific ST-segment and T-wave abnormalities
Right axis deviation
Right bundle-branch block
T-wave inversion in leads V1–V3
P pulmonale (increased P wave amplitude)
S1Q3T3 (large S wave in lead 1, large Q wave in lead 3, and T-wave inversion in lead 3)

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

Respiratory differentials for PE

A

Pneumothorax
Pneumonia
Acute bronchitis
Acute exacerbation of asthma /COPD/chronic lung disease

17
Q

Cardiac differentials for PE

A
Acute coronary syndrome
Acute congestive heart failure
Dissecting or rupturing aortic aneurysm
Unstable angina
Myocardial infarction
Pericarditis
18
Q

Other differentials for PE

A

Musculoskeletal chest pain
GORD
Panic disorder
Any cause of syncope e.g. vasovagal, postural hypotension, arrythmias, seizures, CVD

19
Q

Differentials for pleuritic chest pain (5)

A
Pneumonia
PE
Pneumothorax
Pleurisy
Pericarditis
20
Q

Diagnosing PE

A

History + exam
CXR or ECG to exclude other causes if necessary
ABGs
Well’s score - if >4, arrange immediate CTPA. If less than or equal to 4, arrange D-dimer test. If positive, arrange immediate CTPA.
If there is a delay in getting CTPA, give interim LMWH.

21
Q

What is the PE Well’s score? (7)

A

Clinical features of deep vein thrombosis +3 points

Tachycardia +1.5 points

Immobilization >3 days or surgery in the previous 4 weeks +1.5 points

Previous DVT or PE +1.5 points

Haemoptysis +1 point

Cancer (receiving treatment, treated in the last 6 months, or palliative) +1 point

Alternative diagnosis is less likely than PE +3 points

22
Q

What is the use of V-Q or perfusion scintigraphy in diagnosing PE?

A

May be done in certain circumstances e.g. half-dose perfusion scintigraphy in pregnancy, or if allergy to contrast, or renal impairment
Not very specific (40%)

23
Q

What is the use of echo in diagnosing PE?

A

For people with hypotension (clinically ‘massive’ PE). The absence of right heart failure excludes PE.
?To exclude pericarditis

24
Q

Pharmacological treatment for confirmed PE

A

Low molecular weight heparin
Fondaparinux
Unfractionated heparin
Oral anticoagulant treatment (warfarin, apixaban, or rivaroxaban)
LMWH followed by an oral anticoagulant (dabigatran or edoxaban)

USUALLY LMWH/FONDAPARINUX INITIALLY (for at least 5 days) AND THEN WARFARIN WITHIN 24 HOURS (for at least 3 months)

25
Q

Mechanical treatments may be offered in some cases. What are the options?

A

1) Permanent or temporary IVC filters - trap thromboemboli en route to the pulmonary circulation
2) Thrombolytic therapy - peripheral vein or directly into pulmonary arteries, e.g. streptokinase (plasminogen activators)
3) Open pulmonary embolectomy (surgical removal of clots)

26
Q

What follow up for those with unprovoked PE?

A

Offer investigations to assess for cancer - CXR, FBC, calcium, LFTs, urinalysis, CT scan +/- mammogram if >40yo
Offer antiphospholipid testing
Consider thrombophilia testing

27
Q

Enoxaparin and tinzaparin - mechanism, place in therapy, side effects, monitoring

A

Mechanism = LMWH, activates anti-thrombin III and forms a complex that inhibits thrombin, factors Xa, IXa, XIa, XIIa

Indicated to treat VTE in pregnancy, and in patients with risk factors such as obesity, cancer, recurrent VTE, and in uncomplicated patients with low risk of recurrence.
It is also used for prophylaxis.
Used if PE in cancer.

Side effects - haemorrhage, heparin-induced thrombocytopenia, skin reactions, thrombocytopenia, thrombocytosis, alopecia, hyperkalaemia, osteoporosis, priapism

Monitoring - routine monitoring not recommended,
if so anti-Factor Xa

28
Q

Fondaparinux - mechanism, place in therapy, side effects

A

Mechanism = synthetic pentasaccharide that inhibits activated factor X.
Used for prophylaxis and treatment.
Side effects - anaemia; haemorrhage; chest pain; coagulation disorder; dyspnoea; fever; hepatic function abnormal; nausea; oedema; platelet abnormalities; skin reactions; thrombocytopenia; vomiting; wound secretion

29
Q

Unfractionated heparin - mechanism, place in therapy, side effects

A

Treatment of mild to moderate or severe pulmonary embolism
Also used for prophylaxis in medical and surgical patients, and also in pregnancy

Mechanism - activates anti-thrombin III

Side effects - haemorrhage, heparin-induced thrombocytopenia, skin reactions, thrombocytopenia, thrombocytosis, alopecia, hyperkalaemia, osteoporosis, priapism

30
Q

Warfarin - mechanism, place in therapy, side effects, monitoring

A

Mechanism – inhibits reduction of vitamin K to its active form, which in turns acts as a cofactor in the carboxylation of clotting factor II, VII, IX, X and protein C

Used in prophylaxis and treatment

Side effects –
haemorrhage, alopecia, nausea, vomiting, abnormal LFTs, skin necrosis, skin reactions, pancreatitis, jaundice, blue toe syndrome

Monitoring - INR, target 2.5 or 3.5 if recurrent

Used for 3 months, or 6 months if unprovoked

31
Q

Apixaban, rivaroxaban mechanism

A

Direct factor Xa inhibtior

32
Q

Dabigatran mechanism

A

Direct thrombin inhibitor

33
Q

Management of massive PE

A

ABCDE
Initiate unfractionated heparin
Get ICU input
Thrombolysis = first-line if haemodynamically unstable