Pulmonary Embolism Flashcards

1
Q

What is a pulmonary embolism?

A

Occlusion within the pulmonary arteries

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2
Q

Venous thromboembolism (VTE) is a term that encompasses which two conditions?

A

Deep vein thrombosis (DVT): acute/chronic occlusion of deep vein(s). Commonly affects the lower limbs through the formation of a clot forms (thrombus).

Pulmonary embolism (PE): acute/chronic occlusion of pulmonary arteries. Clot breaks off and travels to the lungs (emboli).

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3
Q

A PE does not always have to be caused by a blood clot. What else can cause it?

A

fat
air
tumour

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4
Q

How is time used to classify the clinical severity of a PE?

acute, subacute, chronic

A

Acute: presentation at onset of vessel occlusion

Subacute: presentation within days or weeks of initial event

Chronic: presentation with complications of chronic emboli (e.g. features of pulmonary hypertension).

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5
Q

What is the meaning of the terms Non-massive, submissive and massive PE?

A

Non-massive: haemodynamically stable and no evidence of right heart strain

Sub-massive: haemodynamically stable, but evidence of right heart strain on imaging (e.g. CT, ECHO) or biochemistry (e.g. elevated troponin)

Massive: haemodynamic instability. Defined as persistently low BP (< 90 mmHg or fall > 40 mmHg) for > 15 minutes or hypotension that requires inotropic support not explained by another cause.

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6
Q

Where is a segmental/subsegmental, lobar and saddle embolism located in the lungs?

A

Segmental and subsegmental: lower order pulmonary vessels. Unilateral or bilateral occlusion

Lobar: right or left main pulmonary arteries. Unilateral or bilateral occlusion

Saddle: embolus lodged at the bifurcation of the pulmonary arteries (3-6% of cases).

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7
Q

What is meaning of a provoked and unprovoked PE?

A

Provoked: transient or persistent risk factors. Typically within three months of event

Unprovoked: seen in 30-50% of cases. No readily identifiable risk factor for VTE.

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8
Q

What is the classical clinical case description that would indicate a PE diagnosis?

A

A history of unilateral leg swelling that precedes the onset of chest pain, dyspnoea and pleuritic chest pain

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9
Q

What are the risk factors for a PE? (7)

State 5 additional risk factors

A

DVT
Previous VTE
Active cancer
Recent surgery (e.g. within last 2-3 months)
Significant immobility (e.g. hospitalisation, bed-rest)
Lower limb trauma/fracture
Pregnancy (+ 6 weeks postpartum)

Additional -
Combined oral contraceptive pill
Long-distance sedentary travel (e.g. long-haul flights)
Thrombophilia
Obesity
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10
Q

Describe the 3 main components of Virchow’s triad use to describe the development of clots

A
  • Venous stasis
  • Hypercoagulable state
  • Endothelial injury
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11
Q

Why does a ventilation/perfusion (V/Q) mismatch develop in pulmonary embolism?

A

Occlusion of one or more of the pulmonary arteries leads to absence of perfusion

ventilation is unaffected - the area of the lung still carries oxygen just no blood

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12
Q

A PE causes decreased blood flow to the affected area of the heart. Classically this should cause an infraction, why may this not happen in PE?

A

bronchial circulation helps to compensate

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13
Q

What are the consequences of a PE and the resultant V/Q mismatch?

A
  • hypoxia and breathlessness
  • elevated pulmonary arterial pressure
  • alveolar collapse
  • worsening hypoxaemia
  • reduction in cardiac output.
  • pulmonary arterial pressure may rise to a level the right ventricle cannot overcome
  • This can lead to hypotension, syncope and right ventricular failure
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14
Q

What are the signs and symptoms of a PE?

A

Symptoms

Dyspnoea (most significant symptom)
Pleuritic chest pain
Cough
Haemoptysis
Dizziness
Syncope
Leg pain and swelling

Signs

Tachycardia (> 100 bpm)
Low grade fever (> 37.5º)
Hypoxia (sats < 94%)

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15
Q

Rights sided hear failure can develop due to PE. Describe the symptoms that can occur is it does

A

Right heart failure

Hypotension (BP < 90 mmHg or drop > 40 mmHg)

Elevated JVP

Tricuspid regurgitation (pansystolic murmur)

Split second heart sound: elevated pulmonary pressure leads to delay in pulmonary valve closure.

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16
Q

Describe the features of a PE WELLS score

A

0-12.5

+3 Sighs and symptoms of a DVT

+3 PE number 1 diagnosis or equally likely

+1.5 Heart rate >100

+1.5 Immobilised >3 days/ surgery within 4 weeks

+1.5 previous DVT/ PE

+1 Haemoptysis

+1 Malignancy +/- treatment <6 months worth of palliative care

17
Q

Describe how the PE wells score is used to guide PE investigations?

A

PE likely (score > 4): straight to computed tomography pulmonary angiography (CTPA), if not available immediately, interim anticoagulation if safe.

PE unlikely (score ≤ 4): d-dimer blood test within four hours. If positive arrange CTPA. If negative, PE excluded consider alternative diagnosis.

18
Q

What is D-dimer?

A

A fibrin-degradation product, which is created when blood clots are broken down by the fibrinolytic system. It is a marker of VTE but can be raised in many conditions.

Very good to exclude PE

But causes a lot of false positives as it is not very specific

19
Q

What is the gold standard investigations for a PE?

A

CTPA

allows visualisation of the pulmonary arterial system with contrast

20
Q

Which investigations are conducted in the investigation of a PE? non imaging

A

ECG

FBC
- FBC
- U&E
- LFT
- Coagulation
- D-dimer
- Arterial blood gas: consider in equivocal cases
Troponin: right heart strain
21
Q

Which imaging tests are being used to investigate a PE?

A

CXR: exclude any obvious alternative pathology that may explain symptoms
CTPA

V/Q scan: nuclear medicine scan that may be utilised in pregnancy or renal impairment

Lower limb ultrasound: confirm presence of DVT

ECHO: assessment of right ventricular strain/failure in patients with suspected ‘massive’ PE.

22
Q

The initial management of a patient with PE is based on what? describe fully

A

Whether the patient is haemodynamically stable or not?

Haemodynamically stable (high-risk): confirmed on CTPA, initiate anticoagulation. High PESI score or features of right heart strain, consider transfer to higher level of care (HDU/ITU).

Haemodynamically stable (low risk): confirmed on CTPA, initiate anticoagulation. Low PESI and no features of right heart strain, consider discharge with anticoagulation follow-up.

Haemodynamically unstable:

  • Shocked low BP patient
  • admitted to a high-dependancy unit (HDU)/intensive treatment unit (ITU).
  • Patients should be considered for thrombolysis
23
Q

Before a PE is confirmed, which anticoagulation therapy is given empirically?

A

LWMH

24
Q

Which anticoagulation therapy is given to a Stable patient with no renal impairment or co-morbidities?

A

offer apixaban/rivaroxaban.

If not-suitable, LWMH for 5 days then offer edoxaban/warfarin

25
Q

Which anticoagulation therapy is given to a Haemodynamic unstable patient with PE?

A

thrombolysis ( tissue plasminogen activator (tPA),- Alteplase) and heparin-based anticoagulation (e.g. unfractionated heparin)

26
Q

Which anticoagulation therapy is given to a patient with active cancer?

A

consider DOAC (e.g. edoxaban). If not suitable, LMWH.

27
Q

Which anticoagulation theraoy is given to a patient with renal impairment?

A

if creatinine clearance (CrCl) 15-50 ml/min, offer apixaban/rivaroxaban or LMWH for 5 days then edoxaban/warfarin

If CrCl <15 ml/min offer LMWH/UFH

28
Q

Describe the meaning of the term bridge therapy

A

If starting warfarin, must have two consecutive INR readings >2.0 before stopping LMWH

29
Q

Which thrombolysis drug is often used in PE?

A

tissue plasminogen activator (tPA)

30
Q

What are the contraindications to thrombolysis?

A

Cardiac arrest with confirmed or suspected PE

Confirmed PE with deterioration despite anticoagulation (i.e. worsening right ventricular strain, increasing oxygen requirements)

Haemodynamic instability (BP < 90 mmHg for > 15 minutes), AND

High clinical suspicious of PE

Confirmed PE within 14 days

31
Q

What is the Long-term management of a PE?

A

Patients are advised to continue anticoagulation for a minimum period of three months.

Beyond three months (3-6 months for active cancer), the duration of therapy depends on whether the PE was provoked or unprovoked, the location of the PE, bleeding risk and whether the underlying risk factor has been removed

In patients with an unprovoked PE, it is important to consider an underlying cause (e.g. inherited thrombophilia, cancer).