Pulmonary Embolism

Question 1

What is an embolism

Answer 1

• The movement of material from one part of the circulation to another.
•  The material may or may not be derived from the circulation itself.
•  Pulmonary embolism means that the material passes through the right side of the heart and lodges in the
pulmonary arteries. Pulmoally usually goes through popliteal vein

Thrombus, tumours air, fat, amniotic fluid, bullet

Question 2

Describe typical PE

Answer 2

•   When we talk about pulmonary embolism in daily practice we mean thrombus entering the right side of the heart and pulmonary arteries
–  90% of PE arise from a deep vein thrombosis (DVT) in the legs, particularly the popliteal vein and more
proximal veins including pelvic veins
–  However, only 25% of patients with a PE have symptoms or signs of a DVT
•   Third commonest cause of vascular death, after
myocardial infarction and stroke •  The commonest cause of preventable death in
hospital patients •  The risk factors are the same as those for DVT

Question 3

What are risk factors for thromboembolism

Answer 3

Most of the factors that precipitate it increase with age. Risk increases with age 
•   Pregnancy 6x
•  Prolonged immobilisation  (3x) 
•  Previous VTE 3x
•  Contraceptive pill 3x
•  Long haul travel (> 4 hrs)  (3x) 
•  Cancer 2.8x
•  Heart failure 2.8x 
•  Obesity 2.4x
•  Surgery > 30 mins 2.3x
•  HRT 2x
•  Thrombophilia - depends on type
• Smoking 1.17x

Question 4

Decsribe presence of risk factors in patients with PE

Answer 4

•   50% have an identifiable ‘temporary’ risk factor (surgery, oestrogen treatment etc…)
•   25% have cancer (permanent risk factor)
•   25% have no identifiable risk factor

Question 5

Describe the main factor pathophysiology of PE

Answer 5

1. Right ventricular overload
   •  Pulmonary artery pressure increases if more than 30% of the total cross section of the pulmonary arterial bed is occluded.
   •  This leads to right ventricular dilatation and strain (think of Frank Starling curve).
   •  Also inotropes are releases in an attempt to maintain systemic BP: these cause pulmonary artery vasoconstriction that further exacerbates the situation.
   •  This is the main cause of death in PE
   •  In about one-third of patients, right to-left shunting through a patent foramen ovale is present and may lead to severe hypoxaemia and an increased risk of paradoxical embolization and stroke

Question 6

What are other factors in the pathophysiology of pe

Answer 6

2. Respiratory failure
   •   Areas of ventilation perfusion mismatch
   •  Low right ventricle output
3. Pulmonary infarction
   •  Small distal emboli may create areas of alveolar haemorrhage
   •  Resulting in haemoptysis, pleuritis, and small pleural effusion
   Not much return circulation - infarction

Question 7

What are the symptoms of PE

Answer 7

Dypnoea 50%, pleuritic chest pain 39%, cough 23%, substernal chest pain 15%, fever 10%, haemolysis 8%, syncope 6%, unilateral leg pain 6%

Question 8

Wha are some physical signs of PE

Answer 8

•   Obvious dyspnoea
•   Tachycardia
•   Low BP
•   Raised JVP (due to RV failure)
•   Pleural rub in cases of pulmonary infarction (pleurisy occurs after pulmonary infarcion)
•   Look for evidence of DVT

Question 9

What are th differential diagnoses

Answer 9

•   Pneumothorax •  Pneumonia •  Pleurisy •  Musculo-skeletal chest pain •  Myocardial infarction •  Pericarditis

Question 10

What are the investigations

Answer 10

•   Blood gases (only if concerned if quite hypoxic):
–  May show hypoxaemia and hypocapnia (respiratory alkalosis) due to hyperventilation
–  Undertaken if evidence of hypoxia requiring oxygen
•  Chest X-ray:
–  By far the commonest finding in PE is normal
–  May be done to exclude other diagnoses
•   ECG:
–  May show signs of right ventricular strain: T wave inversion in the right precordial leads (V1 - V4 and the inferior leads, II, III and aVF).
–  The ‘classic’ finding is SI QIII TIII
–  Not useful as a primary diagnostic tool

–  D-dimer is a fibrin degradation product, a small protein fragment released into the blood when a thrombus is degraded by fibrinolysis
–  A normal D-dimer effectively rules out PE in those at low likelihood of having a PE
–  In those at high likelihood the negative predictive value of D-dimer is too low to use

Question 11

What is the commonest ecg finding in patients with PE

Answer 11

Comminest inning in patient with PE is sinus tachycardia

Question 12

What is the wells criteria for PE

Answer 12

(Dont have to learn in) see slide for general idea
Tries to take into account factors for patients which might have PE - helps with diagnostic probability, helps to determine next step. If wells score >4, doesn’t matter what d dimer test is
If wells score 04-, less likely. Next step is blood test. D dimer. If d dimer is negative - rules out PE

Question 13

Wat are imaging techniques used

Answer 13

NOT used anymore - histr: — pulmonary angiography
— ventilation perfusion lung scintography - not diagnostic

NOWuse
CT pulmonary angiography CTPA

Question 14

Describe a saddle embolus

Answer 14

See slide

Question 15

What is given to treat pe

Answer 15

If someone is hypoxic give oxygen
•   Immediate heparinisation - blood thin
•  This reduces mortality.
•  Study showed that 26% of patients with PE and no treatment died whereas no death due to PE occurred in the intravenous heparin group
•  IV heparin now superseded by SC Low Molecular Weight Heparin

— when treated earlier, reduces mortality

Question 16

How does heparinisation reduce mortality

Answer 16

1.  Stops thrombus propagation in the pulmonary arteries and allows the body’s fibrinolytic system
to lyse the thrombus
2.  Stops thrombus propagation at the embolic source and reduces the frequency of further pulmonary embolism
3.  It does NOT dissolve the clot

Question 17

Describe treatment of high risk patients

Answer 17

•   Haemodynamic support •  Respiratory support
•  Exogenous fibrinolytics (streptokinase/tPA)- this can lyse the clot
–  Peripheral intravenous
–  Delivered directly via a percutaneous catheter into the pulmonary arteries
•  Percutaneous catheter directed thrombectomy - suck out clot
•  Surgical pulmonary embolectomy - rarely done

Question 18

What happens after initial heparinisation

Answer 18

•   Patients are started on an oral anticoagulant (e.g warfarin) (‘DOAC - direct oral anticoagulant ’ e.g. rivaroxaban now increasing prescribed):
–  For 3 months if there is an identifiable ‘temporary’ risk factor (50%)
–  Indefinitely if cancer (SC Low molecular weight heparin - most effective way of managing) or no identifiable risk factor (50%)

Question 19

What about those patients who cannot be safely
anticoagulated? (e.g have oesophageal varices, previous
haemorrhagic stroke, severe thrombocytopenia)?

Answer 19

IVC filter