5.1 Pulmonary embolism Flashcards
Virchow’s triad
-haemodynamic changes/stasis
-hypercoagulability
-endothelial injury
risk factors for each category of virchows triad
-haemodynamic changes/stasis
-long haul flight
-prolonged immobility
-hypercoagulability
-contraceptives/HRT
-smoking
-cancer (pancreatic,colon)
-thrombophilia
-endothelial injury
-injury/trauma
explain how acute R heart strain can be caused by PE
- LV can’t fully expand so output drops, BP drops
- inotropes (NA/adrenaline) released to raise BP via vasoconstriction, but also vasoconstrictor pulmonary circulation X
- also RV wall thins, damaged so wont conduct electrical impulses properly so can lead to arrhythmias
- also possible PFO opens as RV pressure>LV, so deoxy blood can’t deliver enough O2 to tissues, or clot could pass through systemic circumstances = stroke
PE on CXR
-wedge/ Hampton hump
-maybe nothing visible
clinical signs of PE
-RR>16
-crackles
-HR>100
-murmur if severe
-DVT signs
-cyanosis
-sweating
-low grade fever <39
ECG appearance of PE
-sinus tachy *****
-deep S wave lead 1
-pathological Q wave lead 3
-inverted T wave lead 3 (RV strain)
-RBBB
-non specific ST changes
positive predictive value or D dimers
poor
could be raised in pregnancy, surgery, heart disease, trauma
first line imaging for PE suspicion
CXR
when would CTPA be contraindicated?
-pregnancy
-poor renal function
-allergy to dye
what’s involved in a CTPA?
radio opaque dy should fill all pulmonary arteries, dark areas i.e. polo mint view = clot
first treatment for PE
oxygen
do we thrombolyse PE?
not unless its a massive one
thrombolysing treatments
streptokinase
tPA
danger of anticoagulants
heparin induced thrombocytopenia
how does HIT occur?
- antibodies to heparin form nd bind heparin-platelet complexes
- platelets activated and clump, thrombi form and propagate
- spread throughout body = stroke, MI, ishaemia
longer term treatment of PE
-anticoagulants for low risk patients
-if severe:
haemodynamic support
respiratory support
thrombolysis
what constitutes a severe PE?
massive submissive PE
-affects CO so that systolic BP <90
-evidence of heart damage e.g. RV strain, even if systolic BP>90
how long would patients be on oral anticoagulants for after discharge?
3 months if identifiable and preventable risk factor
indefinitely if no identifiable risk, or cancer
who can’t you prescribe anticoagulants to?
-oesophagael varices
-previous haemorrhage stroke
-severe thrombocytopenia
how would you treat someone with recurrent PE despite anticoagulation?
vena cava filter, prevents progression to PE
prevention techniques for each category of virchows triad
-haemodynamic changes/stasis
-AES stockings
-mobilisation
-intermittent pneumatic compression
-hypercoagulability
-anticoagulants
-endothelial injury
-falls prevention
-avoud necessary invasive procedures
most common cause of pulmonary infarction
PE
explain how PE causes pulmonary infarction
occlusion of distal pulmonary artery, -bronchial arteries are recruited as new primary source of perfusion for pulmonary capillaries
-higher blood pressure of bronchial arteries increases capillary blood flow
-erythrocytes extravasate (alveolar haemorrhage)
-tissues necroses and infarct
