6. Pulmonary Embolism Flashcards

1
Q

What are the 3 primary influences that predispose a patient to blood clot formation?

A

Endothelial injury
Stasis or turbulence of blood flow
Blood hypercoagulability

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2
Q

What are the risk factors for thromboembolism?

A
Pregnancy
Prolonged immobilisation
Previous VTE
Contraceptive pill
Long haul travel
Cancer
Heart failure
Obesity
Surgery >30 mins
HRT
Age
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3
Q

What are the hypercoagulable conditions?

A

Antithrombin III deficiency
Protein C or protein S deficiency or restart
- factor V Leiden mutation causing resistance to activated protein C
Lupus anticoagulant
Homocystinuria
Occult neoplasm
Connective tissue disorders

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4
Q

What is the pathophysiology of clinical outcomes in PE?

A

Acute right ventricular overload/failure - leads to cardiogenic shock and/or cardiac arrest secondary to arrhythmias
Respiratory failure - due to areas of ventilation perfusion mismatch
Pulmonary infarction - areas of alveolar haemorrhage, results in haemoptysis, pleuritic and small pleural effusion

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5
Q

What are the symptoms in PE?

A
Dyspnoea
Pleuritic chest pain
Cough
Substernal chest pain
Haemoptysis
Syncope 
Leg pain
Fever
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6
Q

What are the signs of PE?

A
Tachypnoea
Rales or decreased breath sounds
Accentuated second heart sound
Tachycardia
Fever
Diaphoresis
Lower extremity oedema
Cardiac murmur
Cyanosis
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7
Q

What are the differential diagnoses of the signs and symptoms of PE?

A
Pneumothorax
Pneumonia
MI
Pericarditis
Pleurisy
MSK chest pain
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8
Q

What does an ABG show in PE?

A

May show hypoxaemia an hypocapnia due to hyperventilation

Sometimes PaO2 may be normal

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9
Q

What does a CXR show in PE?

A

Often it is completely normal
May be done to rule out other diagnoses
May show wedge shaped pleural based infiltrate

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10
Q

What does an ECG show in PE?

A

May show signs of right ventricular strain - T wave inversion in right precordial leads
Classic findings are deep S wave in lead I, Q wave in III, inverted T wave in III
Prone to supraventricular tachyarrhythmias

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11
Q

What do D dimer investigations show in PE?

A

A normal D dimer effectively rules out PE in those at low likelihood of PE, not high
+ve D dimer, do further imaging

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12
Q

What is the treatment of PE?

A

Give O2

Immediate heparinisation

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13
Q

How does heparinisation reduce mortality?

A
  1. Stop thrombus propagation in pulmonary arteries and allows body’s fibrinolytic system to lyse the thrombosis
  2. Stops thrombus propagation at embolism source and reduces frequency of further PE
  3. Does not dissolve clot
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14
Q

What do you need to watch out for after heparinisation?

A

Heparin-induced thrombocytopenia

  • body produces antibodies to a portion of heparin
  • low platelet count
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15
Q

What is the treatment for heparin-induced thrombocytopenia?

A

Immediate cessation of all formulations of heparin

Need to use non-heparin based anti-coagulant

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16
Q

What is the treatment of high risk PE patients?

A
Haemodynamic support
Respiratory support
Exogenous fibrinolytics 
Percuatneous catheter directed thrombectomy
Surgical pulmonary embolectomy
17
Q

What happens after initial heparinisation?

A

Patients stated on an oral anticoagulant e.g. warfarin or DOAC

18
Q

What do you do if you cannot use any form of anti-coagulation for PE?

A

Inferior vena cava filter

19
Q

Who would you use an inferior vena cava filter on?

A

Large haemorrhagic CVA
Large oesophageal bleed
Retroperitoneal bleed

20
Q

How do you prevent DVT/PE in inpatients?

A

DVT prophylaxis after surgery

DVT prophylaxis for patients with malignancy