1. PULMONARY EMBOLUS Quick revision guide – Chris Scott

2. Plan  Presentation  Risk Factors  Investigation  Treatment

3. Risk Factors  Think Virchow’s Triad  Endothelial Wall (damage) Hypertension  Flow (stagnation) / Turbulence Recent travel (flights, car journeys) / immobility Mitral stenosis Varicose Veins  Viscosity (coagulability) Hormonal contraception / HRT DIC Smoking AT3 / Protein S deficiency Nephrotic Syndrome Severe Trauma & Burns Ca (Pregnancy)

4. Presentation  Acute onset SOB  Pleuritic chest pain  Haemoptysis  Collapse  Tachycardia  Hypotension  Tachypnoea / Dyspnoea  Pleural Rub  Cyanosis SymptomsSigns More often than not clinically silent

5. Investigations  ECG  ABGs – most likely show a respiratory alkalosis  CXR  Bloods – primarily to exclude other causes of chest pain / respiratory distress  FBC (anaemia, infection)  U+E – Check renal function prior to drugs  LFT – Warfarin may be used, to check hepatic function  D-Dimer’s  Lower limb dopler – most common origin of the embolus is a DVT  V/Q Scan  CTPA

6. Investigations - ECG  Usually just tachycardia, sometimes incomplete RBBB  Rarely, the classical signs of Right Heart Stress – the S1Q3T3 Pattern – but has been only demonstrated in those patients in whom we already have a high index of clinical suspicion of PE  S-wave in lead 1  Q-wave in lead 3  T-wave inversion in lead 3

7. Investigations – ECG Example S1 Q3 T3 Tachycardia

8. Investigations - CXR Hampton’s HumpWestermark’s Sign A wedge shaped lung infarct after a PE Reduced pulmonary vascular markings

9. Investigations – D-Dimers  Product of cross-linked fibrin degradation in vivo  High sensitivity  Low specificity  High negative predictive value  Low positive predictive value  Therefore useful in ruling out PE but not great at diagnosing Conditions causing raised D-dimers PE DVT DIC Postoperatively Any breakdown of clots

10. V/Q & CTPA  V/Q Scan – involves inhaling radioactive gas and being injected with a different radioactive isotope (separately) and measured with a Gamma Camera. They are then compared for mismatch.  CTPA - best on the larger, proximal pulmonary arteries. Used if V/Q is equivocal or contraindicated

11. Treatment  Usual structure of Conservative, Medical, Surgical  Conservative – unacceptable  Medical – anticoagulation  Surgical – IVC mesh; thrombectomy  Mainstay of treatment – anticoagulation for 3-6 months  Initially Heparin (LMW Heparin) and long term Warfarin

12. Heparin  Route: IV  Mechanism:Cofactor for AT 3 – an endogenous inhibitor of thrombin  Monitoring: APTT  In overdose – protamine sulphate

13. Warfarin  Route: PO  Mechanism:Vitamin K analogue – competative inhibition of of VKOR (Vitamin K Epoxide Reductase)  inhibitor of gamma-glutamyl carboxylase activity  Reduction of VitK Dependent clotting factors (II,VII, IX, X)  Monitoring: INR  In overdose – Vitamin K / Beriplex/ FFP

14. Heparin Warfarin