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
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
3
Q
What percentage of pulmonary embolisms arise from lower limb DVTs?
A
- 90%
4
Q
What is the pathophysiology of pulmonary embolism?
A
- Haemodynamic changes/stasis
- Endothelial injury/dysfunction
- Hypercoagulability
5
Q
What are the types of embolism?
A
- Thrombus
- Fat
- Gas (air)
- Amniotic fluid
- Foreign material
6
Q
What are the risk factors of pulmonary embolism that cause stasis of blood?
A
- Prolonged immobility
7
Q
What are the risk factors of pulmonary embolism that cause stasis of blood and vessel wall damage?
A
- Peri-operative
- Varicose veins
8
Q
What are the risk factors of pulmonary embolism that cause vessel wall damage?
A
- Injury/trauma
- Vascular access (iatrogenic)
9
Q
What are the risk factors of pulmonary embolism that cause hypercoagulability?
A
- Cancer
- Smoking
- Thrombophilia
- Oestrogen containing medication
10
Q
What are the risk factors of pulmonary embolism that cause stasis/turbulence and hypercoagulability?
A
- Pregnancy
- Obesity
11
Q
What are the risk factors of pulmonary embolism that cause stasis/turbulence and hypercoagulability and vessel wall damage?
A
- Increasing age
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
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%
14
Q
What is the impact of PE?
A
- Acute right heart strain
- Respiratory failure
- Pulmonary infarction
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
16
Q
What can acute right ventricular overload lead to?
A
- Death due to:
- Cardiogenic shock with circulatory failure
- Cardiac arrest due to arrhythmias
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
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
What investigations do we need to do to diagnose PE?
- Rule in/out differential diagnoses
- ECG
- Blood tests
- Imaging
26
Why is an ECG helpful when considering PE as a diagnosis?
- Helps rule out MI
- Classic findings seen for PE (though may also seem completely normal)
27
What are the classic ECG findings for PE?
- Deep S wave in lead I
- Pathological Q wave in lead III
- Inverted T wave in lead III
28
What other findings may be seen on an ECG when someone has a pulmonary embolism?
- Sinus tachycardia (most common abnormality)
- Right bundle branch block
- Right ventricular strain
- Non-specific ST changes
29
What blood tests are done when trying to diagnose a PE?
- ABG
- FBC, U&E, CRP, troponin (rule out other differentials)
- D-dimer
30
What is D-dimer?
- 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
What do we mean when we say that D-dimer has a high negative predictive value in low risk patients?
- If PE is unlikely, negative D dimer rules it out
32
If a patient has low risk of VTE, does the D dimer result affect whether we do imaging or not?
- Yes - result determines whether imaging is needed
33
If a patient has high risk of VTE, does the D dimer result affect whether we do imaging or not?
- No - must skip straight to imaging
34
What imaging is done to help diagnose PE?
- CXR
- CTPA is gold standard
- V/Q scan used if CTPA is contraindicated
35
How is PE treated?
- 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
Which anticoagulants can be given to treat PE?
- 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
What is HIT?
- 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
What further treatments are given to patients with PE?
- Low risk patients discharged with anticoagulants
- Severe cases require haemodynamic support, respiratory support, thrombolysis/surgical intervention
39
Patients are usually switched to an oral anticoagulant for discharge. But for how long?
- 3 months if identifiable temporary risk factor
- Indefinitely if no identifiable risk factor or cancer
40
What conditions might contraindicate anticoagulants?
- High bleeding risk due to:
- Oesophageal varices
- Previous haemorrhagic stroke
- Severe thrombocytopoenia
- Recurrent PE despite anticoagulation
41
How is stasis/turbulence treated following PE?
- AES (compression stockings)
- Mobilisation
- Intermittent pneumatic compression
42
How is hypercoagulability treated following PE?
- Anticoagulants
43
How is vessel wall damage treated following PE?
- Falls prevention
- Avoid unnecessary invasive procedures
