s5. pulmonary embolism Flashcards
what can embolise
air fat amniotic fluid thrombus -blood clot tumour
how does DVT get to lungs
enter right ventricle, pulmonary artery into pulmonary circulation to lungs
virchow’s triad
- endothelial injury
- stasis or turbulent blood flow
- blood hypercoagubility
> risk factors for thromboembolism
risk factors for thromboembolism
reasons why
-pregnancy> higher oestrogen state, fetes compress pelvic veins > stasis
- immobilisation
- previous VTE
- contraception pill > produce more clotting factors
- long haul travel> stasis/ turbulence legs bent
- cancer (pancreatic particularly)> inflammation
- heart failure> stasis and sedentary
- obesity
- surgery
- thrombophillia> condition where blood is hypercoaguable
- severe burns> inflammation and imobilised
- COVID 19 > virus invades endothelium leading to endothelial injury AND high inflammation state
list of some hypercoaguable conditions
- antithrombin 2 deficiency
- protein C or S deficiency (anticoagulation proteins)
- Factor v lieden mutation (most common)
- lupus anticoagulant
- homocystinuria
- occult neoplasm
- connective tissue disorders e.g. rheumatoid arthritis
describe factor V Leiden deficiency
causes resistance to activated protein C > which is own body anti coagulant
it means that clot propagation continues as activated protein C doesn’t inhibit factor 5 (clotting factor)
**most common risk factor of DVT/PE in young people
genetic- can be homo or heterozygous
complication of PE-acute right ventricular overload
acute right ventricular overload
- right sided heart failure leading to left sided
1) usually RV pumps blood into low pressure system. low resistance
2) obstruction causes right sided strain as resistance increases
3) CO and BP falls > to compensate body raises systemic BP > inc pulmonary artery vasoconstriction and exacerbates the problem
> cardiogenic shock
main cause of death from PE
cardiogenic shock with circulatory failure
cardiac arrest secondary to arrhythmias
complications with patent foramen ovale and PE
right to left shunting through the patent foramen ovale
> bakcup of blood. by passing lungs. no gas exchange
> severe hyperaemia and inc risk of paradoxical embolisation (bits of clot move thru arterial system) and stroke
complication of PE- respiratory failure
due to areas of ventilation perfusion mismatch
low right ventricle output
complication of PE - pulmonary infarction
small distal emboli may create areas of alveolar haemorrhage
> result in haemoptysis, pleuritic and small pleural effusion (pulmonary infarction)
* may be visible on CXR as wedge shape
symptoms of PE
- dyspnea (difficulty breathing)
- pleuritic chest pain (sharp, stabbing, gets worse with inspiration)
- cough
- substernal chest pain
- haemoptysis (coughing up blood)
- fever (low grade not really high temp)
- syncope (fainting)
- unilateral leg pain
signs of PE
- tachypnea (high resp rate over 16/min)
- decreased breath sounds
- accentuated second heart sound (Created by closing of aortic and pulmonic valve)> pulmonic sounds louder coz right ventricle working harder
- tachycardia
- low grade fever
- diaphoresis (sweating)
- lower extremity oedema
- central cyanosis (Caused by the hyperaemia and VQ mismatch)
main differential diagnoses PE
- pneumothorax (pleuritic chest pain. SOB)
- pneumonia
- MI (pain is usually crushing/ radiating but can have atypical chest pain that presents like PE)
- pericarditis
- pleurisy (pleuritic chest pain. dyspnea)
- musculoskeletal chest pain (pleuritic chest pain)
investigations for PE- what do blood gases show
- hyperaemia and hypocapnia due to hyperventilation
> high CO2 so pH increases therefore respiratory alkalosis.
