Pulmonary Embolism Flashcards

1
Q

What is an embolism?

A

The movement of material from one part of the circulation to another.

The material may or may not be derived from the circulation itself.

Pulmonary embolism means that the material passes through the right side of the heart and lodges in the pulmonary arteries.

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2
Q

What could be embolisms?

A
Thrombus 
Tumour
Air
Fat
Amniotic fluid 
Bullet
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3
Q

What is a pulmonary embolus?

A

Thrombus entering the right side of the heart and pulmonary arteries.

90% of PE arise from a DVT in legs, particularly popliteal veins and more proximal veins including pelvic veins.

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4
Q

What percentage of patients with a PE have evidence of a DVT?

A

Only 25% of patients with a PE have symptoms or signs of a DVT.

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5
Q

What is the commonest cause of preventable death in hospital patients?

A

PE

It is also the thrust commonest cause of vascular death after MI and stroke.

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6
Q

What are the risk factors for thromboembolism?

A
Over 55 
Pregnancy (6x)
Prolonged immobilisation (3x)
Previous VTE (3x)
Contraceptive pill (3x)
Long haul travel (3x)
Cancer (2.8x)
Heart failure (2.8x)
Obesity (2.4x)
Surgery - over 30mins (2.3x)
HRT (2x)
Thrombophilia 
Smoking (smaller risk but still increased)
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7
Q

What % of patients with a PE present with risk factors?

A

50% = identifiable temporary risk factors (e.g. surgery, oestrogen treatment ect..)

25% = cancer (permanent risk factor)

25% = non-identifiable risk factor

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8
Q

What is the risk of sudden death from a PE?

A

20%

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9
Q

3 phases of pathophysiology of PE

A
  1. Right ventricular overload
  2. Respiratory failure
  3. Pulmonary infarction
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10
Q

Why does right ventricular overload cause a PE?

A

Pulmonary artery pressure increases if more than 30% of the total cross section of the pulmonary arterial bed is occluded.

This leads to right ventricular dilation and strain

Also inotropes are released in an attempt to maintain systemic BP: these cause pulmonary artery vasoconstriction that further exercerbates the situation. -Main cause of death in PE.

In about 1/3 of patients, a patent foramen ovale is present and may lead to severe hypoxaemia and an increased risk of paradoxical embolisation and stroke.

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11
Q

Why does a PE create resp failure or pulmonary infarction?

A

Resp failure - areas of ventilation perfusion mismatch = low right ventricle output.

Pulmonary infarction -smal distal emboli may create areas of alveoli haemorrhage which results in haemoptysis (coughing up blood), pleuritis and small pleural effusion.

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12
Q

What are the symptoms of a PE?

A

Dyspnoea (breathlessness) -50%

Pleuritic chest pain -39%

Cough -23%

Substernal chest pain -15%

Fever -10%

Haemoptysis (coughing up blood) -8%

Syncope -6%

Unilateral leg pain -6%

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13
Q

What are the physical signs of a PE?

A

Obvious dyspnoea

Tachycardia

Low BP

Raised JVP

Pleural rub incase of pulmonary infarction

Evidence of DVT

BUT, could also be no signs.

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14
Q

What are the main differential diagnoses of a PE?

A

Pneumothorax

Pneumonia

Pleurisy

Muscle-skeletal chest pain

Myocardial infarction

Pericarditis

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15
Q

What investigations would you do if you suspect a PE?

A

Blood gases

  • May show hypoxaemia and hypocapnia (respiratory alkalosis) due to hyperventilation)
  • Undertaken If evidence of hypoxia requiring oxygen

Chest X-Rays

  • By far the commonest finding in PE is normal
  • May be done to exclude other diagnoses

ECG
-Signs of right ventricular strain: T wave inversion in right pericordial leads (V1-4 and II,III, aVF)
-The classic finding is S1, Q3, T3
But not useful as a primary diagnostic tool
Most common finding is sinus tachycardia.

D-dimer

  • D dimer is a fibrin degredation product, a small protein fragment released into the blood when a thrombus is degraded by fibrinolysis.
  • A normal D-dimer effectively rules out PE in those at a low likelihood of having a PE.
  • In those at a high likelihood, the negative predictive value of D-dimer is too low to use.
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16
Q

What is the Wells score?

A

A score you can look at to work out the likelihood of a PE.

17
Q

What imaging would you do for a PE?

A

Pulmonary angiography (old) - take a history instead

Ventilation persuasion lung scintigraphy (old -take a history instead)

CTPA - CT Pulmonary Angiography (this is what is done now)

18
Q

How do you treat a PE?

A

Oxygen!

Immediate heparinisation - reduces mortality by thinning blood.

Give low molecular weight heparin (based on weight)

19
Q

How does heparinisation reduce mortality?

A

Strop thrombus propagation in the pulmonary arteries and allows the body’s fibrinolytic system to lyse the thrombus.

Stops thrombus propagation at the embolic source and reduces the frequency of further pulmonary embolism.

It does NOT dissolve the clot.

20
Q

How do you treat high risk patients with a PE?

A

Haemodynamic support

Respiratory support

Exogenous fibrinolytics (streptokinase / tPA) -Peripheral intravenous, delivered via a percutaneous catheter into the pulmonary arteries. This will lyse the clot!

Percutaneous catheter directed thrombectomy

Surgical pulmonary embolectomy.

21
Q

What happens after the initial heparinisation?

A

Started on oral anticoagulants - used to be warfarin but not as much anymore.

If cancer - long term low molecular weight heparin

If bleeding problem and not safely anti-coagulated - IVC filter - collect clots coming up from the legs.

22
Q

What do you give to patient who are in hospital and are at risk of a PE?

A

Given prophylactic load dose heparin - mostly older people who are unwell.