Pulmonary Embolism

Question 1

Pathogenesis of PE.

Answer 1

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.

Question 2

Risk factors/Causes of PE.

Answer 2

Recent surgery, especially abdominal/pelvic or hip/knee replacement.

Thrombophilia

Leg fracture

Prolonged bed rest/reduced mobility

Malignancy

Pregnancy/postpartum/COCP

Previous PE/DVT

Question 3

Clinical features of PE.

Answer 3

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

Question 4

Signs of PE.

Answer 4

Pyrexia

Cyanosis

Tachypnoea

Tachycardia

Hypotension

Raised JVP

Pleural rub

Pleural effusion

Question 5

Investigations of PE.

Answer 5

Bloods - FBC, U&Es, baseline clotting, D-dimers

ABG

CXR

ECG

Question 6

Investigating suspected PE without shock or hypotension.

Answer 6

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.

Question 7

Investigating suspected PE with shock or hypotension.

Answer 7

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.

Question 8

Features of Wells score.

Answer 8

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

Question 9

Initial treatment of PE.

Answer 9

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.

Question 10

Management of large pulmonary embolism.

Answer 10

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.

Question 11

Clinical features of massive PE.

Answer 11

Hypotension/imminent cardiac arrest

Signs of RH strain on CT/ECHO

Consider thrombolysis with IV alteplase

Question 12

Absolute thrombolysis CIs.

Answer 12

Haemorrhagic or ischaemic stroke within 6 months

CNS neoplasia

Recent trauma or surgery

GI bleed < 1 month

Bleeding disorder

Aortic dissection

Question 13

Relative thrombolysis CIs.

Answer 13

Warfarin

Pregnancy

Advanced liver disease

Infective endocarditis

Question 14

Thrombolysis complications.

Answer 14

Bleeding

Hypotension

Intracranial haemorrhage/stroke

Systemic embolisation of thrombus

Reperfusion arrhythmias

Allergic reaction

Question 15

What options are there to switch to long term anticoagulation?

Answer 15

Warfarin

DOAC

LMWH

Question 16

What is the target INR for warfarin?

Answer 16

2-3

Question 17

When switching from DOAC/LMWH to warfarin what do you need to think about?

Answer 17

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.

Question 18

What is the first line long term anticoagulation for when a patient is pregnant or in malignancy?

Answer 18

LMWH

Question 19

How long should you continue long-term anticoagulation for?

Answer 19

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)

Question 20

If CTPA is unavailable what can be used instead?

Answer 20

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.

Question 21

ECG features of PE

Answer 21

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.