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Respiratory Core Conditions > 2+ Pulmonary Embolism > Flashcards

2+ Pulmonary Embolism Flashcards

1
Q

What is the definition of a PE?

A

Obstruction of one or more of the pulmonary arteries by solid, liquid or gaseous masses (usually a DVT from the leg)

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2
Q

What age group are most likely to get a PE?

A

> 65

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3
Q

What are the risk factors for PE?

A
  • Increasing age
  • DVT
  • Surgery in last 2mo
  • Bed rest >5 days
  • Previous VTE
  • FamHx
  • Recent trauma or fracture
  • Active malignancy
  • Pregnancy/post-natal period, high oestrogen states (obesity, OCP, HRT)
  • Hypercoagulable states
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4
Q

What are some inherited risk factors for PE/DVT?

A

Hypercoagulable states!
- Factor V leiden mutation
- Prothrombin G20210A mutation
- Antithrombin deficiency
- Protein S deficiency
- Protein C deficiency
- Anti-phospholipid syndrome

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5
Q

Where do most emboli causing PE come from?

A

Lower limb proximal veins (iliac, femoral, popliteal) –> through the right ventricle –> pulmonary arteries: lodges

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6
Q

What are the aetiological sources of PE?

A

Thrombus (from deep veins)= most
Gas emboli
Fat from a fracture

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7
Q

What is the aetiology of a thrombus?

A

Virchow’s Triad!!

  1. Vessel wall damage
  2. Venous stasis
  3. Hypercoagulability
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8
Q

How does vessel wall damage contribute to virchow’s triad and what causes it?

A

Endothelial cell damage promotes thrombus formation, usually at venous valves

  • Trauma
  • Previous DVT
  • Surgery
  • Venous harvest
  • Central venous catheterisation
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9
Q

How does venous stasis contribute to virchow’s triad and what causes it?

A

Poor blood flow and stasis promote formation of a thrombi + congestion causes valvular damage –> further promotes thrombus formation

  • Age >40
  • Varicose veins
  • Immobility
  • GA
  • Paralysis
  • Spinal cord injury
  • Myocardial infarction
  • Prior stroke
  • Adv CHF
  • Adv COPD
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10
Q

How does hypercoagulability contribute to virchow’s triad and what causes it?

A

Promotes thrombus formation. Inherited and acquired causes

  • Cancer
  • High oestrogen states
  • IBD
  • Nephrotic syndrome
  • Sepsis
  • Blood transfusion
  • Inherited thrombophilia
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11
Q

What is the pathophysiology of a PE?

A

Once the embolus has lodged it results in:

  1. Decreased gas exchange: due to mechanical obstruction of the vascular bed –> V/Q mismatch –> hypoxia
  2. Infarction where the clot lodges in smaller pulmonary arteries –> pleuritic chest pain
  3. Cardiovascular compromise: depends where the clot is but you can have compromised CO –> hypotension
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12
Q

What is a saddle PE?

A

If the embolus is large enough it can lodge in the main pulmonary artery and obstruct flow from the right ventricle to the lung

Life threatening!

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13
Q

What is the clinical presentation of a PE?

A

Symptoms:
- Dyspnoea
- Cough
- Pleuritic chest pain
- Haemoptysis
- Calf pain or swelling (DVT symptoms)

Ex:
- Tachypnoea
- Tachycardia
- Hypoxia
- Signs of DVT
- If saddle PE or massive PE: low BP, signs of RHF (raised JVP, leg swelling)

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14
Q

What is the diagnostic algorithm for suspected PE?

A
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15
Q

What is the Well’s Score for PE?

A
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16
Q

Brief Summary of what Ix you do for a PE?

A

Bedside:
- ECG

Labs:
- FBC
- D-dimer
- Baseline coags
- UEC
- Trop
- BNP
- LFTs
- Do a thrombophilia screen

Imaging:
- CXR
- CTPA
- V/Q scan
- Lower limb compression venous USS if concerned for DVT

17
Q

What bedsides Ix do you do for PE?

A

ECG
- Mostly sinus tachy
- Can have S1Q3T3
- New RBBB

18
Q

What laboratory Ix do you do for PE?

A
  • FBC
  • D-dimer (elevated)
  • Baseline coags (need this to be able to start anti-coags)
  • UEC (need baseline when prescribing anti-coags + may need contrast)
  • Trop (rule out ACS)
  • BNP (rule out CHF)
  • LFTs (can influence anti-coag choice)
  • Thrombophilia screen if PE is unexplained, FamHx, or cough change the Mx
19
Q

What imaging do you do for PE?

A

CXR:
- Mostly to rule out other causes
- Can see a Hampton’s hump (increased dome-shaped opacity in the lower lobe) from haemorrhage

CTPA:
- Most sensitive and specific
- Often see wedge shaped infarctions with pleural effusion

V/Q Scan:
- Pulmonary artery occlusion leads to ventilated areas without perfusion (dead space)

Lower limb compression venous USS if suspect a DVT

20
Q

WHat’s included in the thrombophilia screen?

A
  • Factor V Leiden mutation
  • Prothrombin G20210A mutation
  • Antithrombin deficiency
  • Protein S deficiency
  • Protein C deficiency
  • Anti-phospholipid syndrome
21
Q

What is the DDx of PE?

A

CHF
MI
Pneumonia
Exacerbation of chronic lung disease
Pericarditis
MSK pain
Valvular insufficiency

22
Q

What is the overall Mx of PE?

A
  • 45 degrees sitting position
  • Oxygen supplementation
  • IV fluid resuscitation
  • DVT prophylaxis required in future (some people need IVD filter if anti-coags are contra-indicated)

Other Mx depends on whether hemodynamically stable or unstable

23
Q

What is the management of someone who is hemodynamically stable with a PE?

A

1st Line: Use a NOAC/DOAC (apixaban or rivaroxaban) as they don’t need parenteral anticoagulation for initiation
- Also don’t need routine anticoagulation monitoring
- If using Dabigatran, lead in with LMWH for 5 days then stop before starting

2nd line: if you can’t use a NOAC/DOAC (pregnancy, cancer, severe kidney impairment), use warfarin + parenteral or LMWH

24
Q

How do you manage a subsegmental PE?

A

Management is controversial and varies but surveillance rather than anticoagulation is considered teh best option for most patients

25
Q

How do you manage a haemodynamically unstable patient with a PE?

A
  1. Start UFH
  2. Thrombolysis: alteplase, streptokinase, urokinase
  3. After UFH, switch to apixaban or rivaroxaban (LMWH if those unsuitable)
  4. CONSIDER a vasopressor (noradrenaline) or inotrope (dobutamine) if systolic BP remains <90 after thrombolysis

CONSIDER: surgical embolectomy/percutaneous treatment

26
Q

What are complications of PE?

A
  • Pulmonary infarction (localised necrosis of lung tissue –> frequent when distal vessels are occluded)
  • Acute bleeding during treatment
  • Recurrent venous thromboembolic event
  • Cardiac arrest from right ventricular collapse due to massive embolism
  • Chronic thromboembolic pulmonary hypertension

Respiratory Core Conditions (7 decks)

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