Lecture 10: Pulmonary embolism Flashcards

1
Q

What is an embolism?

A

Obstruction of a blood vessel by a forgein substance or blood clot that travels through the bloodstream, loding in a vessel and plugging it.

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2
Q

What can embolise?

A
  • thrombus
  • tumour
  • air
  • fat
  • amniotic fluid
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3
Q

What is a pulmonary embolism?

A

The material passes through the right side of the heartand lodges in the pulmonary arteries

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4
Q

Where do pulmonary embolisms usually arise from?

A

DVT in the legs, particularly the popliteal vein and more proximal veins, including pelvic veins
-you can have no symptoms of DVT

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5
Q

What are the risk factors for a thromboembolism?

A
Virchow's triad
-endothelial injury
-stasis or turbulence of blood flow
-blood hypercoagulability
(you can have more than one)
  • pregnancy
  • prolonged immobilisation
  • contraceptive pill
  • long haul travel
  • cancer
  • heart failure
  • obesity
  • previous venous thrombolic embolism
  • surgery >30mins
  • thrombophilia
  • hormone replacement therapy
  • age
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6
Q

What can a DVT cause?

A
  • stroke
  • pulmonary embolism
  • heart attack
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7
Q

How do you treat DVT/pulmonary embolisms?

A

Anticoagulants

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8
Q

What is the presence of risk factors in patients with PE?

A

-50% have an identifiable ‘temporary’ risk factor
-25% have cancer (pancreatic cancer most common for DVT/PE)
-25% no indentifiable risk factor
If someone has a DVT with no risk factor, you need to consider if there is an undetected malignancy

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9
Q

What are some hypercoagulable conditions (except pregnancy)?

A
  • antithrombin 3 deficiency
  • protein C or S deficiency causing resistance to activated protein C is most common risk factor for DVT/PE in young people
  • lupus anticoagulant
  • homocystinuria
  • occult neoplasm
  • rheumatoid arthritis (connective tissue disorders)
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10
Q

What is the outcome after a PE?

A
  • sudden death (20%)
  • respiratory failure (due to areas of V/Q mismatch/low right ventricular output/shunt via patent foramen ovale)
  • pulmonary infarction (not as common as lungs receive blood from systemic system as well)
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11
Q

How does a PE cause acute right ventricular overload?

A
  • pulmonary artery pressure increases if more than 30% of the total cross section of it is occluded
  • leads to acute right ventricular dilatation and strain
  • inotropes are released by the body to maintain systemic bp, causing pulmonary artery constriction which exacerbates the situation
  • also the increased pumping of the right ventricle pushes on the left ventricle and makes the EDV lower, this leads to cardiogenic shock
  • it also can cause arrythmias, which can lead to cardiac arrest
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12
Q

Why is a patent foramen ovale dangerous?

A

Right to left shunting through a patent foramen ovale

-leads to hypoxaemia and increased risk of paradoxial embolisation and stroke

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13
Q

What symptoms do you get in PE?

A
Common
-dyspnoea
-pleuritic chest pain (when you take a deep breath in)
-cough
Rarer
-substernal chest pain
-syncope
-unilateral leg pain
-haemoptysis (coughing of blood)
-low grade fever
-chest wall tenderness on palpation 

(may have no symptoms)

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14
Q

What signs do you see in PE?

A
  • tachypnoea (resp rate <16)
  • decreased breath sounds
  • accentuated second heart sound (pulmonary valve which you don’t usually hear, but you do here because right side is working harder)
  • tachycardia
  • fever
  • diaphoresis (sweating)
  • lower extremity oedema
  • caridac murmur
  • cyanosis
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15
Q

What are the main differential diagnoses for PE?

A
  • pneumothorax
  • pneumonia
  • MI
  • pericarditis
  • pleurisy (fluid in pleura)
  • musculo-skeletal chest pain
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16
Q

How do we investigate for a PE?

A

Blood gas
-hypoxaemia and hypocapnia due to hyperventilation
-to see if they require oxygen
CXR
-usually normal
-done to exclude other diagnoses
-classic finding is a peripheral wedge shape (infarction)
ECG
-show signs of right ventricular strain
-deep S wave in lead 1, Q wave in lead 3, inverted T wave in lead 3
-could have supraventricular tachyarrhythmias
D-dimer
-this is a fibrin degredation product released into the blood when a thrombus is degraded by fibrinolysis
-a normal D-dimer rules out PE in those at a low risk (not high risk)

17
Q

What is the clinical probability score for DVT/PE?

A

Help to stratify people into different risk categories, so the most appropriate diagnostics/treatments can be followed

Wells score

  • likely (>4): imaging is recommended
  • unlikely (0-4): D-dimer test
18
Q

What imaging do you do for a PE?

A

CT pulmonary angiography (CTPA)

19
Q

How do you treat for a PE?

A
  • Oxygen

- immediate heparinisation (subcutaneous low molecular weight heparin)

20
Q

How does heparinisation reduce mortality?

A
  1. stops thrombus propagation in pulmonary arteries and allows body’s fibrinolytic system to lyse the thrombus
  2. stops thrombus propagation ar embolic source and reduces the frequency of further pulmonary embolism
    It does not dissolve the clot, the body does this
21
Q

What is heparin induced thrombocytopenia?

A

Body produces antibodies to a portion of heparin that also recognise heparin-platelet complexes, the binding of antibody to platelts activates them and platelet clumps are formed leading to thrombi: LEADS TO THROMBOCYTOPENIA (less platelets)
-these are little microemboli which can cause infarcts in venous/arterial system

22
Q

How do you treat heparin induced thrombocytopenia?

A

Immediate cessation of heparin

-use non-heparing based anti-coagulant

23
Q

How do you treat high risk PE patients?

A
  • haemodynamic support
  • respiratory support
  • exogenous fibrinolytics (streptokinase): delivered directly via percutaenous catheter into pulmonary arteries
  • percutaneous catheter directed thrombectomy
  • surgical pulmonary embolectomy
24
Q

What happens after initial heparinization?

A

-start on oral anticoagulant (warfarin/DOAC) for 3 months if there is an identifiable temporary risk factor, or indefinitely if it is cancer or no indentifiable risk factor
(some patients can’t be safely anticoagulants: oesophageal varices, previous haemorrhagic stroke, severe thrombocytopenia)

25
Q

What do you use if you can’t use an form of anti-coagulant?

A

Use inferior vena cava filter (body ends up forming collaterals eventually around this)