Pulmonary Embolism Flashcards
Pathogenesis of PE.
Usually arise from a venous thrombosis in the pelvis or legs.
The clot breaks off and pass through the veins and the riht side of the heart before lodging in the pulmonary circulation.
Risk factors/Causes of PE.
Recent surgery, especially abdominal/pelvic or hip/knee replacement.
Thrombophilia
Leg fracture
Prolonged bed rest/reduced mobility
Malignancy
Pregnancy/postpartum/COCP
Previous PE/DVT
Clinical features of PE.
Difficult diagnosis and have a lot of differentials.
Small emboli can be asymptomatic, large are often fatal.
Acute breathlessness
Pleuritic chest pain
Haemoptysis
Dizziness
Syncope
Signs of PE.
Pyrexia
Cyanosis
Tachypnoea
Tachycardia
Hypotension
Raised JVP
Pleural rub
Pleural effusion
Investigations of PE.
Bloods - FBC, U&Es, baseline clotting, D-dimers
ABG
CXR
ECG
Investigating suspected PE without shock or hypotension.
Assess clinical probability by two-levels Wells score.
< 4 (low risk) -> do D-dimer
> 4 (high risk) -> immediate CTPA or treat empirically DOAC (apixaban or rivaroxaban) if there is a delay of the CTPA. If CTPA is positive -> diagnosis confirmed.
If the D-dimer is negative consider an alternative diagnosis.
If the D-dimer is positive then immediate CTPA or empirical treatment with LMWH.
Investigating suspected PE with shock or hypotension.
CTPA straigh away.
+ve -> treat
-ve -> look for differentials
If CTPA is not available then bedside echocardiography.
If there is RV dysfunction/overload treat as if PE.
If -ve echocardiography search for other causes.
Features of Wells score.
Clinical signs and symptoms of DVT - 3 points
HR > 100 bpm - 1.5
Recently bed-ridden or major surgery - 1.5
Previous DVT or PE - 1.5
Haemoptysis - 1
Cancer receiving active tx - 1
An alternative diagnosis is less likely than PE - 3
Initial treatment of PE.
ABCDE
Oxygen if hypoxic
Fluid resuscitiation if hypotensive.
If good story and signs -> make the diagnosis. Start treatment before definitive investigations (need to check for contraindications). This is because most PE deaths occur within 1 hour.
Commence DOAC like apixaban or rivaroxaban. LMWH if contraindicated or antiphospholipid syndrome.
Management of large pulmonary embolism.
O2 if hypoxic 10-15L/min
Morphine 5-10mg IV if in pain and distress.
IV access and start DOAC like apixaban or rivaroxaban.
If BP drops give 500 ml IV fluid bolus and get ICU input
If haemodynamically unstable consider thrombolysis such as alteplase 10mg IV bolus then IVI 90mg/2h and then initiate long-term anti-coag.
If haemodynamically stable consider vasopressors like dobutamine 2.5-10 mcg/kg/min IV or noradrenaline to aim for a systolic BP of >90 mmHg and then initiate long-term anti-coag.
Clinical features of massive PE.
Hypotension/imminent cardiac arrest
Signs of RH strain on CT/ECHO
Consider thrombolysis with IV alteplase
Absolute thrombolysis CIs.
Haemorrhagic or ischaemic stroke within 6 months
CNS neoplasia
Recent trauma or surgery
GI bleed < 1 month
Bleeding disorder
Aortic dissection
Relative thrombolysis CIs.
Warfarin
Pregnancy
Advanced liver disease
Infective endocarditis
Thrombolysis complications.
Bleeding
Hypotension
Intracranial haemorrhage/stroke
Systemic embolisation of thrombus
Reperfusion arrhythmias
Allergic reaction
What options are there to switch to long term anticoagulation?
Warfarin
DOAC
LMWH
What is the target INR for warfarin?
2-3
When switching from DOAC/LMWH to warfarin what do you need to think about?
Continue LMWH for 5 days or when the warfarin is in its therapeutic range (INR 2-3) for 24-48h.
Continue DOAC for 2 days and can be discontinued when warfarin is in its therapeutic range (INR 2-3) for 24-48h.
What is the first line long term anticoagulation for when a patient is pregnant or in malignancy?
LMWH
How long should you continue long-term anticoagulation for?
3 months if there is an obvious reversible cause (then review)
Beyond 3 months if the cause is unclear, there is recurrent VTE or there is an irreversible underlying cause such as thrombophilia. This is often 6 months in practice.
6 months in active cancer (then review)
If CTPA is unavailable what can be used instead?
Ventilation-perfusion (VQ) scan
With a pulmonary embolism there will be a deficit in perfusion as the thrombus blocks blood flow to the lung tissue. This area of lung tissue will be ventilated but not perfused.
Patients with a pulmonary embolism often have a respiratory alkalosis when an ABG is performed. This is because the high respiratory rate causes them to “blow off” extra CO2. As a result of the low CO2, the blood becomes alkalotic. It is one of the few causes of a respiratory alkalosis, the other main cause being hyperventilation syndrome. Patients with a PE will have a low pO2 whereas patients with hyperventilation syndrome will have a high pO2.
ECG features of PE
Sinus tachycardia (most common)
Complete or incomplete RBBB
Right ventricular strain pattern – T wave inversions in the right precordial leads (V1-4) ± the inferior leads (II, III, aVF).
Right axis deviation
Dominant R wave in V1
Right atrial enlargement (P pulmonale) – peaked P wave in lead II
SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T wave in III. This “classic” finding is neither sensitive nor specific for pulmonary embolism; found in only 20% of patients with PE.
