Flashcards in PE Deck (69):
What are symptoms of PTE?
SOB, collapse, pleuritic chest pain, heamoptysis and sudden death.
What are the signs of PE?
Tachypnoea, wheeze, pleural rub and signs of pleural effusion
hypotension, tachycardia, arrest and fourth heart sound,
Oligemia (water mark) on CXR.
What investigations do we do for PE?
ABG's and D dimers.
CXR, VQ scan and CTPA (CT pulmonary angiogram).
echo, angiography and ECG.
What is the time frame for doing a VQ scan in PE?
What is a con of the test?
Within 48 hours of event.
It is poor at discriminating between PE and background lung disease
What is a CTPA? How is it done and what are the disadvantages?
CT pulmonary angiogram.
Inject IV contrast and get to hold breath.
It is poor for peripheral lesions.
What are we looking for in an echo for PE?
Right sided heart strain and pressures.
What are the objectives of PE treatment?
Prevent post thrombotic syndrome.
Prevent recurrent venous thromboembolism.
Minimise side effects and inconvenience.
What is the recommended treatment for a massive PE?
Thrombolysis or surgery.
What is the recommended treatment for a minor PE with RV dysfunction?
Anticoagulants and thrombolysis.
What is the recommended treatment for a major PE without RV dysfunction?
What is the recommended treatment for a minor PE?
What anticoagulants do we give for PE?
LMWH and warfarin.
Initial treatment with LMWH.
Induction period with LMWH of 5 days is associated with a lower rate of recurrent PE.
Stop heparin when INT is greater than 2.
Optimal range of warfarin therapy is still to be established. Should continue for at least 3 months.
What thrombolytic therapy do we use for PE?
What are the effects of TPA on PE?
Accelerates resolution but has no effect on the extent of resolution. No effect on frequency of recurrence and may reduce subsequent pulmonary HT.
What are the indications for an IVC filter?
Recurrent PE despite anti coagulation.
PE When anti coagulation cannot be used
High risk thrombolysis of DVT e.g. Plegmasia dolens.
What surgery do they do for PE?
Endartectomy for chronic thromboembolic pulmonary hypertension.
What vitamin K antagonists do we use for PE?
Warfarin and phenindone
What are new oral anti thrombin agents we can use for PE?
Dabigatran and anti XA e.g. Apixaban and rivaroxaban.
What is UFH?
What are two heparin analogues?
Hirudins and danaparoid.
What are the mechanisms of action of anticoagulants?
Prevent clot formation and extension.
What are the mechanisms of action of anti platelet drugs?
Interfere with platelet activity.
What are the mechanisms of action of thrombolytic agents?
Dissolve existing thrombi.
What are the indications for warfarin?
Post MI, recurrent MI, stroke or systemic embolisation.
Prevention and treatment of cardiac embolism.
Prophylaxis and/or treatment of:
Venous thrombosis and its extension.
Thrombolytic complications associated with AF and cardiac valve replacement.
How do we calculate INR?
Patients PT in seconds divided by mean normal PT in seconds.
Multiply this answer by the international sensitivity index.
What are contradictions to warfarin therapy?
Risk of haemorrhage greater than benefit of treatment.
Uncontrolled alcohol/drug abuse.
What patient education should we give about anticoagulation?
Teach safety, discuss regular INR, counsel on other medications, alcohol and diet. Discover strategies for improving compliance.
How does heparin work?
Heparin binds to thrombin inactivating it - inefficiently.
Also activates anti thrombin which in turn inactivates thrombin efficiently.
Also inactivates factors XA, iXa and XIa.
How do we monitor heparin?
Activated partial thromboplastin time. APTT.
What does UFH do?
Large molecule, cross links thrombin with antithrombin.
Thrombin inhibition 4 fold compared to action on factor Xa.
It is unpredictable and must be monitored.
How does LMWH work?
Small molecule, no cross links.
Thrombin inhibition 1 to 1 with action on Xa
Predictable by weight and doesn't need monitoring.
How do we dose LMWH? What is this effective in?
Once daily subcut.
Effective in DVT.
Treatment of PE effective and safe.
Compare LMWH and UFH?
LM has less osteopenia and HIT then UFH.
Outpatient treatment safe and effective.
What increases the risk of bleeding with anticoag therapy?
Aged over 65 years, past GI bleeding, MI, anaemia, renal failure and DM.
What are potential indicators for indefinite anticoag therapy?
Recurrent idiopathic VTE.
Thrombolembolic pulmonary hypertension.
What do we need to monitor when we give factor Xa inhibitors?
What do we need to monitor when we give anti-thrombin drugs?
What is the reversibility of dabigatran?
Elimination half life 12-17 hours.
Drug cessation usually sufficient.
What do we use if we must reverse dabigatran?
Recombinant factor VIIa.
All remove 60% within 3 hours.
What is the reversibility of FXa inhibitors?
Drug cessation usually sufficient.
Elimination half life 5-9 hours.
What do we do if we must reverse FXa inhibitors?
Prothrombin complex concentrate. Reliably and completely reverses FXa.
What are the classifications of acute PE (thrombo)? What do they present with?
Massive - shock or syncope.
Major with right ventricular dysfunction.
Major with normal right ventricular function.
What is an embolus?
Detached intra vascular mass carried to a site in the body distant from its origin.
What two important things can PE's cause?
Sudden death and pulmonary hypertension.
What type of emboli are most common?
What is the most common source of pulmonary emboli?
DVTs of lower limb.
What are the three parts of virchows triad?
Stasis, vessel wall damage and hypercoagulability.
What are two typical patient populations that suffer from hypercoagulability?
MI and cancer patients.
What are the risk factors for PE?
Contraceptive pill and HRT
Pulmonary hypertension and vasculitis.
What are the most and least likely lower limb DVTs to embolise?
Most likely are proximal e.g. Ileofemoral. Least likely are distal e.g. Popliteal.
What factor does the clinical presentation of PE depend on?
The size of the emboli.
How does a large PE present?
How do medium size PEs present?
Pleuritic pain, hameoptysis and breathlessness.
How do small recurrent PE's present?
Progressive dyspnoea, pulmonary hypertension and right sided heart failure.
What will we see in ABG results for PE?
PaO2 decreased and decreased sats.
E.g. Type 1 respiratory failure PaCO2 normal or low.
What can we expect to see in a CXR for PE?
Can be normal early on before infarction.
After infarction we can see basal actelectasis, consolidation and pleural effusion.
Why do we do an echo for PE?
To measure the pulmonary artery pressure and look for hypertrophy.
What will we see on a VQ scan before and after infarction?
Before infarction there will be a perfusion defect.
After there will be a perfusion Dan ventilation matched defect.
If we cannot find an obvious cause for PE what should we think about?
How can we prevent DVT?
Early mobilisation after surgeries.
Calf muscle exercises.
Subcut low dose molecular heparin.
What will we see on a VQ scan for recurrent PEs?
Multiple filling defects which are mismatched to ventilation.
What might we see on an angiogram for massive PE?
Occluded right main pulmonary artery and filling defect in the left pulmonary artery.
What should we expect to see on an ECG for PE?
Signs of acute right heart strain e.g. Inverted T waves in V1-3.
Does aspirin have a role in the treatment of PE? Why?
No as it is an anti platelet drug.
What kind of half lives do both warfarin and LMWH have?
If we over anticoagulate someone how do we treat them?
Address underlying cause.
Maybe cover with FFP or other blood factors.
How do we reverse warfarin?
With vitamin K1.
How do we reverse heparin?