Pulmonary embolism Flashcards
Define pulmonary embolism
Pulmonary embolism (PE) is a consequence of thrombus formation within a deep vein of the body –> occluding the pulmonary vasculature
Thrombus formation in the venous system occurs as a result of:
- venous stasis
- trauma
- hypercoagulability
What are the 3 factors:
- venous stasis
- trauma
- hypercoagulability
collectively known as?
Virchow’s triad
Approx what % of deep venous thrombi will embolise to the pulmonary vasculature, resulting in a PE?
Approx. 51%
Where is the most common site of venous thrombus formation?
lower extremities.
What is venous thromboembolic disease?
The preferred term to describe the spectrum of disease
- beginning with the risk factors of Virchow’s triad
- progressing to deep venous thrombosis
- resulting in life-threatening PE
What may be the consequences of a PE if it is not aggresively treated?
- RHF
- cardiac arrest
What is the aetiology of pulmonary embolism
Virchow’s triad:
- venous stasis
- trauma (vessel wall damage)
- hypercoagability
Venous stasis:
- poor blood flow and stasis promote the formation of thrombi.
- Venous stasis and congestion result in valvular damage, further promoting thrombus formation.
Vessel wall damage:
- endothelial cell damage promotes thrombus formation, usually at the venous valves.
Hypercoagulability:
- a number of other conditions (both inherited and acquired) increase the risk of PE.
Which factors/conditions are associated with venous stasis?
- age >40 years
- immobility
- general anaesthesia
- paralysis
- spinal cord injury
- MI
- prior stroke
- varicose veins
- advanced congestive heart failure
- advanced COPD.
What are the insults that can cause venous vessel wall damage?
- trauma
- previous DVT
- surgery
- venous harvest
- central venous catheterisation
Do venous thrombi occur de novo in the pulmonary vasculature?
rarely
- Clots usually form in the deep venous system of the lower extremities and embolise.
Why might a PE cause RHF?
- PE occurs when a thrombus dislodges and becomes trapped in the pulmonary vasculature.
- This obstruction increases pulmonary vascular resistance (PVR), increasing the work of the right ventricle.
- The right ventricle compensates by increasing heart rate using the Frank-Starling preload reserve via dilation.
- Further increases in PVR overcome the right ventricular (RV) compensatory mechanisms, leading to over-distension of the right ventricle, increased RV end-diastolic pressure, and decreased RV cardiac output.
- Decreased RV output leads to decreased left ventricular (LV) preload.
- As left ventricle filling and cardiac output decrease, lowered mean arterial pressure progresses to hypotension and shock. In previously healthy individuals, this can occur when as little as 50% of the pulmonary vasculature is occluded.
What do DVTs consist of?
DVTs are composed mainly of fibrin and entrapped erythrocytes (red clots)
- Unlike platelet-rich arterial thrombi
Hence endothelial damage appears to be less important in DVT than in arterial thrombosis.
Although platelet aggregation is seen, it is not evident at the site of thrombus attachment, suggesting that activation of the coagulation cascade precedes platelet activation
Recall the coagulation cascade

Recall how platelets are activated

Which conditions (both inherited and acquired) increase the risk of hypercoagulability?
- cancer
- high-oestrogen states (oral contraceptives, hormone replacement, obesity, pregnancy)
- IBD
- nephrotic syndrome
- sepsis
- blood transfusion
- inherited thrombophilia (factor V Leiden mutation, prothrombin gene mutation, protein C and S deficiency, antithrombin deficiency, and antiphospholipid antibody syndrome).
What are the strong risk factors of pulmonary embolism?
PMH
-
cancer
- multiple myeloma, brain and pancreatic cancer = highest RR
- lung, colon, and prostate cancer = most episodes
-
Recent surgery or hospitalisation
- Lower limb fractures and joint replacements = strongest provoking factors
-
Previous or current DVT
- present in 25% pts with PE
-
Pregnancy and 6 weeks postpartum
- = 4x risk of thrombosis during pregnancy
- = 60x risk after pregnany vs non-pregnant women
SH
- History of immobilisation
What are the weak risk factors for a PE?
PMH
-
Other significant medical comorbidities
- e.g. congestive heart failure, COPD, concurrent sepsis
- Obesity
- increasing age
- varicose veins
- Known thrombophilias
-
other
- Central vein catheter, Nephrotic syndrome, Chronic dialysis, Myeloproliferative disorders, Paroxysmal nocturnal haemoglobinuria, Behcet’s disease, Blood transfusion
SH
- Long-distance travel
- Smoking
DH
- Combined oral contraceptive pill
- HRT
FH
- 1st-degree relative with a history of confirmed PE or DVT
What % of PEs occur with no underlying risk factors?
30% of cases
can be spontaneous
Summarise the epidemiology of pulmonary embolism
- UK: 47,594 cases of PE were reported in the 1-year period between 2013 and 2014
- higher in older age groups
What are the symptoms of pulmonary embolism?
- dyspnoea
-
peuritic chest pain
- acute onset
- localised to one side of the chest
- unlikely to be central
- (caused by pleural irritation due to distal emboli causing pulmonary infarction)
- cough
-
pain & swelling leg
- commonly 1 leg, although both legs may be affected
uncommon
- fever
-
haemoptysis
- ensure it is true, and not originating from elsewhere
What is the nature of onset of PE symptoms?
acutely rather than gradually
What are the signs of pulmonary embolism o/e?
- tachypnoea
-
hypoxaemia
- Oxygen saturations <94%
- but only presents in 60% of cases
-
creps O/A
- explains cough
- There may also be evidence of a concurrent DVT*
- UNCOMMON: signs of shock/hypotension or severely reduced haemodynamic reserve*
What are the signs of shock/hypotension or severely reduced haemodynamic reserve?
shock:
- altered cognition
- cool extremities
- mottled or ashen skin
- slow capillary refill
- oliguria.

What score is used to assess the risk of PE?
Wells score
- used to assess the likelihood of a PE in any non-pregnant patient who is haemodynamically stable



