Lecture 22 - PE Flashcards

1
Q

Pulmonary embolism

A

Obstruction of a blood vessel by a foreign substance distal to the site of origin

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2
Q

Embolus substances

A
Thrombus
Tumour
Amniotic fluid 
Fat - fracture of long bones 
Air 
Bullet
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3
Q

Fat embolism syndrome

A

Triad of lung, brain and skin

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4
Q

How can fat embolism to the brain

A

Via a patent foramen ovale

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5
Q

Where do most PEs arise from

A

90% arise from DVTs

25% of those have symptoms of DVT

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6
Q

Risk factors for PE

A

Endothelial injury
- surgery

Stasis or turbulent blood flow

  • immobile
  • long haul flight
  • heart failure

Blood hypercoagulabilty

  • COCP
  • inherited disorders e.g thrombophilia
  • cancer (pancreatic)
  • obesity
  • pregnancy
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7
Q

Factor Xa

A

Factor Xa activates fibrin from fibrinogen to form a clot

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8
Q

Hypercoaguable conditions

A
Antithrombin III deficiency 
Protein C or S deficiency/ resistance (anticoagulants)
Lupus anticoagulant
Homocystinuria 
Occult neoplasm
Chronic inflammation e.g RA
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9
Q

How does a PE cause right ventricular overload

A
  1. Pulmonary artery hypertension if more than 30% occlusion
  2. High right ventricle afterload
  3. Right ventricle hypertrophy
  4. Eventually the right ventricle will dilate
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10
Q

Inotropes

A
  • Right sided heart failure decreases blood pressure due to decreased venous return.
  • inotropes are released to increase blood pressure by causing systemic vasoconstriction
  • pulmonary artery vasoconstriction further increases right sided afterload
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11
Q

Main cause of death in PE

A
  • cardiogenic shock with circulatory failure

- cardiac arrest secondary to arrhythmias

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12
Q

PE with patent foramen ovale

A
  • Due to the increased pressure in the right ventricle, blood flows from right to left
  • causes cyanosis and hypoxaemia
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13
Q

Paradoxical embolism

A

Embolus carried from the venous system to the arterial system
Occurs due to patent foramen ovale

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14
Q

How does PE cause respiratory failure?

A
  • areas of ventilation perfusion mismatch
  • low right ventricle output
  • shunt with patent foramen ovale
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15
Q

Pulmonary infarct

A

Not common as lungs have a collateral circulation

  • small distal emboli create areas os alveolar haemorrhage
  • haemoptysis, pleuritis, small pleural effusion
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16
Q

Symptoms of PE

A

Common:
Dyspnoae
Pleuritic chest pain

Less common:
Cough
Haemoptysis
Syncope

17
Q

Signs of PE

A

Tachypnoea (16+)
Decreased breath sounds
Accentuated second heart sounds (P2) - pump against resistance
Tachycardia (100+)

18
Q

Investigations

A

ABG

  • hypoxaemia
  • hypocapnia - respiratory alkalosis due to hyperventilation

Oxygen saturation

CXR

  • NORMAL
  • exclude other diagnosis

ECG - not diagnostic

Blood tests
- D-dimer raised - if normal can rule out if low risk for PE

19
Q

ECG

A
  • right ventricle strain (broad complex QRS)
  • supraventricular tachycardia
  • T wave inversion in lead III
  • deep S wave in Lead I
  • Q wave in Lead III
20
Q

Imaging for PE

A

Invasive:
Pulmonary angiogram
Ventilation perfusion lung scintigraphy

Non invasive:
CT pulmonary angiography
- high specificity and sensitivity

21
Q

Saddle pulmonary embolism

A

Large pulmonary embolism that partially occludes the bifurcation of the pulmonary trunk therefore affects the left and right pulmonary artery

22
Q

Treatment of low risk PE patient

A

Oxygen
Immediate IV heparinisation
Oral warfarin

23
Q

How does heparin treat PE

A

Stops propagation of embolism

Allows body’s fibrinolytic system to lose the embolus

24
Q

Risk of heparin use

A

Heparin induced thrombocytopenia

25
Q

Treatment of high risk patients

A
Oxygen 
Haemodynamic support 
Exogenous fibrinolytics e.g streptokinase (can only use once)
Thrombectomy 
Embolectomy