Pulmonary Embolism

Question 1

What are the 2 types of PE?

Define each of them.

Answer 1

Massive PE - “PE associated with a systolic BP of <90 mmHg, or a drop in systolic BP of 40+ mmHg in <15 minutes”

Sub-massive PE - “any PE not meeting the above criteria”

Question 2

List 8 (non-genetic) risk factors of PE.

Answer 2

Surgery <12 weeks previously
Immobilisation for 3+ days in previous 4 weeks
Previous DVT or PE
Family history
Lower limb fracture
Pregnancy/post-partum
Long distance travel
Oestrogen-containing OCP

Question 3

List 6 genetic risk factors for PE.

Answer 3

Factor V Leiden mutation
Protein S deficiency
Protein C deficiency
Prothrombin G20210A mutation
Hypercysteinaemia
Antithrombin deficiency

Question 4

Describe the clinical features of PE.

What are the symptoms? (5)

What are the signs O/E? (5)

Answer 4

SYMPTOMS:
Pleuritic pain
Dyspnoea
Cough
Haemoptysis
Syncope

SIGNS O/E:
Tachypnoea
Crackles
HR 100+ 
Fever 37.8C
Peripheral signs of DVT

Question 5

What are the 2 stages of PE pathophysiology?

Answer 5

Acute changes

Compensatory changes

Question 6

Describe the pathophysiology of acute changes in PE. (4)

Answer 6

1. Blockage of the pulmonary vascular bed causes increased pulmonary vascular resistance
2. This causes right ventricular strain (with possible dilatation)
   a. Right ventricle compensates by increasing heart rate
   b. This reduces right ventricle output
3. This causes a decreased left ventricular preload, therefore decreased left ventricular cardiac output
   a. This causes reduced arterial oxygen content
4. This causes an increased alveolar-arterial gradient
   a. Indicates hypoxaemia

Question 7

Describe the compensatory mechanisms in PE. (3)

Answer 7

1. Blood clot in pulmonary arteries is partially broken down
   a. Right ventricular function recovers
2. Pulmonary artery pressure is increased to allow increased perfusion in poorly ventilated areas
   a. BUT, this causes decreased perfusion in well ventilated areas
   b. This causes increased amounts of dead space due to V/Q mismatch
3. Decreased surfactant production in obstructed zones causes atelectasis
   a. This causes further hypoxaemia

Question 8

Which 6 investigations would you do for PE?

Answer 8

Blood tests, including:

• D-dimers
• ABGs
• Troponin

ECG

Echocardiogram

CXR

CT pulmonary angiogram

V/Q scan

Question 9

What features of PE would you see on blood tests? (2)

Answer 9

Elevated D-dimers

Respiratory alkalosis on ABGs

Question 10

What features of PE would you see on an ECG? (5)

Answer 10

Tachycardia
AF
S1Q3T3 pattern
Right ventricular strain
Right bundle branch block

Question 11

How would you treat massive PE? (3)

Answer 11

Unfractionated heparin (IV)

Fluid resuscitation

Thrombolysis (alteplase)

Question 12

How would you treat sub-massive PE? (3)

Answer 12

LMWH, e.g. dalteparin (subcut)

Switch to oral anti-coagulants, continue for 3 months (e.g. DOACs, warfarin)

Lifelong oral anti-coagulation therapy if recurrent PE

Question 13

What is atelectasis?

Answer 13

Failure of the lung to expand

Question 14

Describe the S1Q3T3 pattern on ECG. (3)

Answer 14

Deep S wave in lead I
Q waves in lead III
Inverted T waves in lead III