Pulmonary Embolism (PE) Flashcards
Where do PE come from?
Anywhere in venous system
90% systemic veins
10% R.Heart
Majority are Abdominal in origin.
DVT also common
Axillary not uncommon
Rare emboli materials (not VTE)
Fat
Tumour
Foreign Body
Amniotic Fluid
Virchow’s Triad of thrombus formation
Hypercoagubility
Endothelial Injury
Disturbed Blood flow
Risk Factors PE
Reduced mobility: post surgery / comorbidity / long haul travel / Functional Active Ca Ca treatment >60yrs Age Dehydration Thrombophillias Obesity FH HRT/Oestrogen usage Long Bone fractures IV drug usage Pregnancy DVT Varicose vein Phlebitis
Pathophysiology PE
lung tissue distal to embolus is ventilated but not perfused
Increase in dead space and decrease in Gas exchange
Ventilation/ perfusion mismatch
Lung tissue denatures shortly (and eventually necroses) and stops producing surfactant causing alveolar collapse
decreases area of pulmonary arterial bed increasing P arterial pressure
decreases cardiac output
Types of PE
- Asymptomatic (60% of people will have micro-emboli)
- Common PE
- Massive PE (CO affected)
Presentation of common PE
Sudden unexplained breathlessness
sometimes accompanied by pleuritic pain, heamoptysis and signs of DVT
TACHY, LOCALISED PLEURAL RUB AND COARSE CRACKLES, PYREXIA
ECG changes in PE
- Sinus Tachycardia (by far most common)
- New onset AF
- Tall peaked P waves (P. Pulmonale) Right axis deviation and R Bundle Branch Block
Massive PE presentation
sudden collapse/ presyncope cardiac chest pain and shock O/E: raised JVP with a wave Gallop rhythm Split Heart Sounds R Ventricular heave
Management of PE
- ABCDE
- Wells Score
- Investigations
- If confirmed PE rest, anticoagulate.
- fibrinolyis or surgery if appropriate
Wells Score for PE
< 3 = unlikely PE. D Dimer to exclude and consider differentials
>4 = Likely PE- CTPA