5.1 Pulmonary Embolism Flashcards
Embolism
Obstruction of blood vessel by foreign substance or blood clot that travels through blood stream, lodging in blood vessel - plugging the vessel
Types of emboli
- Thrombus
- Tumour
- Air - after surgery
- Fat - after trauma
- Amniotic fluid - after labour
Pulmonary embolism
- In daily practice - refers to a thrombus emboli
- Emboli enters right side of heart and pulmonary arteries
- 90% of PE’s arise from DVT’s (most common cause)
- Most preventable and unexpected of hospital deaths
Virchow’s Triad
Increased risk of clotting:
• Endothelial injury - e.g. trauma/surgery
• Stasis/turbulence of blood flow - can cause propogation of clot
• Blood hypercoagulability
• Inflammation can act through any of the three above to predispose an individual to clotting
Hypercoagulability states
- Prior thrombosis
- Immobility
- Malignancy
- DIC
- HRT (Hormone replacement therapy - oestrogens)
- Pregnancy
- Prolonged travel
- Surgery
- Oral contraceptive pill
- Heart failure
- Thrombophilia
- Severe burns
Consequences of PE
- Hypoxaemia - due to V/Q mismatch (>1)
- Right sided heart failure - obstruction of pulmonary circulation causes right sided strain/hypertrophy/failure
- Pulmonary infarction - but rare due to collateral vessels (bronchial arteries) which maintain perfusion slightly
Fat emboli
• Normally resolve spontaneously
• Can give rise to fat embolism syndrome (FES):
- traumatic causes: fracture of femur/pelvis/tibia and or massive soft tissue injury/severe burns/bone marrow biopsy’s etc.
- non traumatic causes: acute pancreatitis / fatty liver / haemoglobinopathies etc.
• Seen as petechial rash, decreased level of consciousness and SOB
Amniotic fluid emboli
- Sudden, unexpected maternal collapse associated with hypotension/hypoxaemia/DIC
- Occurs when amniotic fluid or fetal cells/hair along with other debris enter maternal circulation
- Most cases occur during or immediately after labour
Covid-19
• Risks of venous thromboembolism (VTE) increased with covid-19 (due to severe inflammation)
Hypercoagulable disorders
- Antithrombin III deficiency
- Protein C or S deficiency
- Factor V Leiden mutation - resistance to protein C (anti-coagulation proteins) is the most common risk factor
How does PE: acute right ventricular overload
• Pulmonary artery pressure increases due to PE if >30% of artery is occluded
• Leads to acute right ventricular dilatation and strain
• + inotropes released in attempt to maintain BP:
- increase contractility of heart and constrict pulmonary arteries which worsens condition
- puts more strain on right side of heart
• In about ⅓ of PE patients have patent foramen ovale allowing for right-to-left shunting
- May lead to severe hypoxaemia and paradoxical embolisation (from vein to artery)
How does PE: respiratory failure
- Areas of V/Q mismatch (lower perfusion so V/Q>1)
- Low right ventricle output
- Shunt with patent foramen ovale
- All cause hypoperfusion to the lungs
How does PE: pulmonary infarction
- Small distal emboli may create areas of alveolar haemorrhage
- May result in haemoptysis, pleuritis and small pleural effusion
- May be visible of CXR as wedge shape
Symptoms of PE - most common to least common
- Dyspnoea - SOB
- Pleuritic chest pain - somatic - sharp/localised/acute
- Cough
- Substernal chest pain
- Haemoptysis
- Fever
- Syncope
- Unilateral leg pain
- Chest well tenderness
Signs of PE - most common to least common
- Tachypnoea - increased RR
- Decreased breath sounds
- Accentuated second heart sound (pulmonic artery sound much louder)
- Tachycardia
- Fever
- Diaphoresis (sweating)
- Lower extremity oedema
- Cardiac murmur
- Central cyanosis (due to hypoxaemia)