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Respiratory > Pulmonary embolism > Flashcards

Pulmonary embolism Flashcards

1
Q

What is an embolism?

A
  • Lodging of a blockage inside a blood vessel
  • Can cause partial or total blockage of bloodflow
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2
Q

What is a venous thromboembolism?

A
  • Embolism caused by a thrombus formed in the venous system
  • Thrombi from a systemic vein will travel through right side of heart and impact lungs
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3
Q

What percentage of pulmonary embolisms arise from lower limb DVTs?

A
  • 90%
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4
Q

What is the pathophysiology of pulmonary embolism?

A
  • Haemodynamic changes/stasis
  • Endothelial injury/dysfunction
  • Hypercoagulability
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5
Q

What are the types of embolism?

A
  • Thrombus
  • Fat
  • Gas (air)
  • Amniotic fluid
  • Foreign material
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6
Q

What are the risk factors of pulmonary embolism that cause stasis of blood?

A
  • Prolonged immobility
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7
Q

What are the risk factors of pulmonary embolism that cause stasis of blood and vessel wall damage?

A
  • Peri-operative
  • Varicose veins
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8
Q

What are the risk factors of pulmonary embolism that cause vessel wall damage?

A
  • Injury/trauma
  • Vascular access (iatrogenic)
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9
Q

What are the risk factors of pulmonary embolism that cause hypercoagulability?

A
  • Cancer
  • Smoking
  • Thrombophilia
  • Oestrogen containing medication
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10
Q

What are the risk factors of pulmonary embolism that cause stasis/turbulence and hypercoagulability?

A
  • Pregnancy
  • Obesity
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11
Q

What are the risk factors of pulmonary embolism that cause stasis/turbulence and hypercoagulability and vessel wall damage?

A
  • Increasing age
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12
Q

Not all patients will have identifiable risk factors for pulmonary embolism - what should you do to determine their diagnosis?

A
  • Consider undiagnosed malignancy or hypercoagulable condition
  • Careful history, age appropriate screening
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13
Q

What happens after PE has formed?

A
  • Up to 10% of patients with acute PE die suddenly
  • Untreated, acute PE mortality rate is as high as 30%
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14
Q

What is the impact of PE?

A
  • Acute right heart strain
  • Respiratory failure
  • Pulmonary infarction
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15
Q

How does PE cause acute right heart strain?

A
  • PE is lodged in pulmonary circuit
  • Right heart tries to pump harder to get blood into lungs
  • Lots of back pressure in pulmonary artery
  • Right side of heart gets bigger and more dilated
  • Left side of heart gets squashed because there is reduced room in mediastinum
  • Leads to reduced CO and low BP
  • Inotropes released to increase BP
  • Cause vasoconstriction of pulmonary arterial system
  • Even more pressure for right side of heart to work against
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16
Q

What can acute right ventricular overload lead to?

A
  • Death due to:
  • Cardiogenic shock with circulatory failure
  • Cardiac arrest due to arrhythmias
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17
Q

Some patients have patent foramen ovale. If they have a PE, what can happen?

A
  • Right to left shunting causes severe hypoxia
  • Paradoxical embolization - clot passes into left heart and systemic circulation
  • Causes stroke
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18
Q

How can PE lead to arrhythmias?

A
  • Acute right heart strain
  • Damages right side of heart
  • Electrical conduction disrupted
19
Q

How does PE lead to respiratory failure?

A
  • Low right ventricle output
  • V/Q mismatch
20
Q

How does PE lead to pulmonary infarction?

A
  • Small distal emboli cause alveolar haemorrhage and infarction
  • Causes haemoptysis, pleuritis, small pleural effusion
  • Can sometimes be seen on CXR - wedge or Hampton hump
21
Q

What are the symptoms of a PE?

A
  • Dyspnoea
  • Pleuritic chest pain
  • Diaphoresis
  • Cough
  • Haemoptysis
  • Syncope
  • Unilateral leg pain/swelling
  • Severity of symptoms do not = severity of PE
22
Q

What are the signs of PE?

A
  • Increased resp rate >16/min
  • Crackles/rales due to reduced air entry
  • Increased HR >100bpm
  • Loud P2 sounds
  • Heart murmurs
23
Q

What are signs of DVT?

A
  • Cyanosis
  • Sweating
  • Low grade fever
  • Unilateral leg swelling
24
Q

What are some differential diagnoses for PE?

A
  • Pneumothorax
  • Pneumonia
  • MI
  • Pericarditis
  • Pleurisy
  • MSK chest pain
  • GORD
25
Q

What investigations do we need to do to diagnose PE?

A
  • Rule in/out differential diagnoses
  • ECG
  • Blood tests
  • Imaging
26
Q

Why is an ECG helpful when considering PE as a diagnosis?

A
  • Helps rule out MI
  • Classic findings seen for PE (though may also seem completely normal)
27
Q

What are the classic ECG findings for PE?

A
  • Deep S wave in lead I
  • Pathological Q wave in lead III
  • Inverted T wave in lead III
28
Q

What other findings may be seen on an ECG when someone has a pulmonary embolism?

A
  • Sinus tachycardia (most common abnormality)
  • Right bundle branch block
  • Right ventricular strain
  • Non-specific ST changes
29
Q

What blood tests are done when trying to diagnose a PE?

A
  • ABG
  • FBC, U&E, CRP, troponin (rule out other differentials)
  • D-dimer
30
Q

What is D-dimer?

A
  • Protein fragment, degradation product of fibrin
  • Should be positive (raised) in patients with VTE
  • However can be raised for many reasons - poor positive predictive value
  • High negative predictive value in low risk patients
31
Q

What do we mean when we say that D-dimer has a high negative predictive value in low risk patients?

A
  • If PE is unlikely, negative D dimer rules it out
32
Q

If a patient has low risk of VTE, does the D dimer result affect whether we do imaging or not?

A
  • Yes - result determines whether imaging is needed
33
Q

If a patient has high risk of VTE, does the D dimer result affect whether we do imaging or not?

A
  • No - must skip straight to imaging
34
Q

What imaging is done to help diagnose PE?

A
  • CXR
  • CTPA is gold standard
  • V/Q scan used if CTPA is contraindicated
35
Q

How is PE treated?

A
  • Start with O2
  • Treat the source - i.e. treat clot
  • Anticoagulants
  • Thrombolysis - fibrinolytics: streptokinase or tPA
  • Mechanical removal - via percutaneous catheter, thrombectomy or surgical embolectomy
36
Q

Which anticoagulants can be given to treat PE?

A
  • Warfarin, heparin and DOACs/NOACs
  • Don’t actively break clot down but stop it from propagating
  • Body lyses clot
  • Immediate heparisation reduces PE mortality
  • Now Low molecular weight heparin is given
37
Q

What is HIT?

A
  • Heparin induced thrombocytopoenia
  • Antibodies form against heparin and bind to heparin-platelet complexes
  • Platelets become activated and clump up
  • Thrombi form and propagate
  • Spread throughout body
  • Cause stroke, MI, limb ischaemia
38
Q

What further treatments are given to patients with PE?

A
  • Low risk patients discharged with anticoagulants
  • Severe cases require haemodynamic support, respiratory support, thrombolysis/surgical intervention
39
Q

Patients are usually switched to an oral anticoagulant for discharge. But for how long?

A
  • 3 months if identifiable temporary risk factor
  • Indefinitely if no identifiable risk factor or cancer
40
Q

What conditions might contraindicate anticoagulants?

A
  • High bleeding risk due to:
  • Oesophageal varices
  • Previous haemorrhagic stroke
  • Severe thrombocytopoenia
  • Recurrent PE despite anticoagulation
41
Q

How is stasis/turbulence treated following PE?

A
  • AES (compression stockings)
  • Mobilisation
  • Intermittent pneumatic compression
42
Q

How is hypercoagulability treated following PE?

A
  • Anticoagulants
43
Q

How is vessel wall damage treated following PE?

A
  • Falls prevention
  • Avoid unnecessary invasive procedures

Respiratory (21 decks)

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