Pulmonary Embolism Flashcards

1
Q

Define embolism

A

Blockage of a vessel by a solid, liquid or gas at a site distant from its origin

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2
Q

List the possible material that can be embolised

A

Thrombus, tumour, air, fat, amniotic fluid, bullet

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3
Q

What are risk factors for PE

A
  • Age
  • Surgery > 30 minutes
  • Obesity
  • Cancer
  • Prolonged immobilisation
  • Previous thromboembolism
  • Heart failure
  • Contraceptive pill
  • Pregnancy
  • Long haul travel > 4 hours
  • Thrombophilia
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4
Q

Explain the pathophysiology of PE

A
  1. Right ventricular over load
    • Pulmonary artery pressure increases if more than 30% of the total cross section of the pulmonary arterial bed is occluded
    • Leads to right ventricular dilation and strain
      • Right ventricle has thinner walls - more susceptible to strain
    • Inotropes are released in an attempt to maintain systemic blood pressure
      • Cause pulmonary artery vasoconstriction - further increase pressure in right ventricle
  2. Respiratory failure
    • Due to areas of ventilation perfusion mismatch and low right ventricle output
  3. Pulmonary infarction
    • Small distal emboli can create areas of alveolar haemorrhage resulting in haemoptysis (coughing out blood), pleuritis, and small pleural effusion
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5
Q

Describe how embolitic strokes can occur

A
  • Some patients have right to left shunting through a patent foramen ovale (hole between the atrium of the heart )
    • May lead to severe hypoxaemia and an increased risk of paradoxical embolization and stroke
  • Embolus can move through foramen ovale into brain - stroke
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6
Q

Define a saddle embolus

A

Large thrombo-emboli that straddles pulmonary trunk and blocks both sides of circulation

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7
Q

State the common symptoms of PE

A
  • Dyspnoea (difficult breathing)
  • Pleuritic chest pain
  • Cough
  • Substernal chest pain
  • Fever
  • Haemoptysis
  • Syncope
  • Unilateral leg pain
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8
Q

What are some physical signs of PE

A
  • Pleural rub in cases of pulmonary infarction

- Raised JVP

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9
Q

Outline how PE can be seen on CXR, ECG and D-dimer tests

A
  • Chest x-ray - by far the commonest finding in PE is a normal CXR
    • CXR may be done to exclude other diagnoses - pneumonia, pneumothorax
  • ECG - may show signs of right ventricular strain
    • T wave inversion in the right precordial leads (V1-V4 and the inferior leads)
    • Classic finding - S1, Q3, T3
  • Blood gases - may show hypoxaemia and hypocapnia due to hyperventilation
  • D-dimer - a normal D-dimer effectively rules out PE in those at low likelihood of having a PE
    • In those at high likelihood, the negative predictive value of D-dimer is too low to use
    • D-dimer is a fibrin degradation product - small protein fragment released into the blood when a thrombus is degraded by fibrinolysis
    • D-dimers not normally present in the blood except when the coagulation system has been activated
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10
Q

What imaging techniques can be used to investigate PE

A
  • Chest x-ray
  • CT pulmonary angiography (CTPA)
    • Dye injected into pulmonary arteries and see where blockage occurs
  • Ventilation perfusion scan
    • Inhalation of dye can see areas of the lung which are ventilated
    • IV injection of labelled albumin can see which areas are perfused
      • Determine areas of ventilation perfusion mismatch
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11
Q

What immediate treatment should be given to PE patients

A
  • Give oxygen
  • Immediate heparinisation
    • Stops 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
    • Not thrombolytic!
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12
Q

What further treatment can be give to high risk PE patients

A
  • Haemodynamic support
  • Respiratory support
  • Exogenous fibrinolytics (streptokinase/tPA)
    • Peripheral intravenous
    • Delivered directly via a percutaneous catheter into the pulmonary arteries
  • Percutaneous catheter directed thrombectomy
  • Surgical pulmonary embolectomy
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13
Q

What further treatment is done after initial heparinisation

A
  • Patients are started on an oral anticoagulant (eg. Warfarin)
    • For 3 months, there is an identifiable ‘temporary’ risk factor (50%)
    • Indefinitely if cancer or no identifiable risk factor (50%)
  • For patients who cannot be safely anticoagulated
    • Occurs for patients with oesophageal varices, previous haemorrhagic stroke, severe thrombocytopenia
    • Inferior venal cava filter inserted through jugular vein
    • Prevent clot from reaching heart by acting as an umbrella which opens in the inferior vena cava after insertion
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