Pulmonary Embolism

Question 1

What is the Virchow’s Triad?

Answer 1

Hypercoagubility
Stasis
Trauma

Question 2

What are the signs and symptoms of pulmonary embolism?

Answer 2

Acute breathlessness
Dizziness
Hypotension
Tachycardia
Central cyanosis
Haemoptysis
Pleuritic chest pain
Pyrexia

Question 3

What is the difference between haematemesis and haemoptysis?

Answer 3

Haemoptysis is the coughing up of blood where as haematemesis is the vomiting of blood

Question 4

What are the differential diagnosis of pulmonary embolism?

Answer 4

• Acute exacerbation of asthma
• Acute exacerbation of COPD
• Pneumothorax
• Congestive Heart Failure
• Unstable angina
• Cardiac Tamponade
• Pericarditis
• MI

Question 5

What are the different types of PEs?

Answer 5

• Small recurrent PEs
• Non massive PEs
• Massive PEs

SMALL RECURRENT PEs:

• Multiple small emboli occlude arterioles
• Gradual development of pulmonary hypertension
• Takes time therefore right side of heart compensates leading to right ventricular hypertrophy
• Eventual decompensation - right sided heart failure

MASSIVE PEs:

• Caused by large embolism at a proximal pulmonary artery or bifurication
• Pulmonary circulation compensates by pulmonary hypertension, leading to cor pulmonale
• Blood not passing through lungs decreases input to left ventricle, causing haemodynamic compromise

NON MASSIVE PEs:

• Medium sized embolus occluding a segmented pulmonary artery
• Results in lack of perfusion to that part of lung
• Clinical presentation:

shortness of breath
pleuritic chest pain
crackles
effusions
pleural rub

Question 6

What is the pathophysiology of pulmonary embolism?

Answer 6

The clotting cascade consists of the intrinsic and extrinsic pathway. Both pathways join at the activation of factor X.

INTRINSIC PATHWAY:
- Factor IXa and factor VIIIa form a complex which activates factor X
EXTRICSIC PATHWAY:
- Tissue factor and factor VIIa form a complex which also activates Factor X

Factor Xa and Va then cause the conversion of prothrombin to thrombin. Thrombin converts fibronegen to fibrin, which holds red blood cells together in a clot

• Part of thrombus breaks off to become an emboli
• Travels via the IVC to heart and eventually becomes lodged in a pulmonary vessel
• Causes back pressure leading to right sided heart failure
• There is a drop in SV, CO and hence BP
• Compensatory tachycardia ensues

Question 7

What is atherosclerosis?

Answer 7

• Atherosclerosis occurs in pulmonary vessels and is the process of chronic inflammation affecting the intima of arteries
• It is characterised by the formation of lipid rich plaques in the vessel wall

Question 8

What are the modifiable risk factors of atherosclerosis?

Answer 8

• Smoking
• Hypertension
• Diabetes
• Dyslipidema

There risk factors lead to endothelial dysfunction:

• increased permeability
• release of adhesion molecules

All of this leads to the recruitment of inflammatory cells: monocytes of T cells

Question 9

What is the role of macrophages in atherosclerosis?

Answer 9

• Produce free radicals and drive LDL oxidation
• They engulf LDLs, becoming foam cells
• Foam cells produce growth factors that cause migration of smooth muscle cells from media to intima

Question 10

What are the gold standard investigations for pulmonary embolism?

Answer 10

• VQ scanning
• CT

CTPA stands for CT Pulmonary Angiography. A sensitive and specific test used on high risk and low risk patients with +ve D Dimer

VQ scanning preferred in renal impairment as the dye used in CTPA is nephrotoxic.

=> In cases of no known risk factors:

• Full history, examination, CXR, bloods and urinalysis
• If above 40, do CT abdo & pelvis to exclude malignancy
• If 1st degree relative known to have thrombophilia, consider antiphospholipid and thrombophilia testing

Question 11

What are the investigations for suspected pulmonary embolism?

Answer 11

=> Bloods
FBC, U&E

=> ECG
SINUS TACHYCARDIA

=> CXR
Decreased vascular markings and small pleural effusions. Asked for before CTPA in non- emergency setting to exclude differentials. May show a wedge shaped opacity

=> ABG
Hyperventilation - respiratory alkalosis

=> D Dimer serum levels
Increased (test is +ve)

Question 12

What is the investigation of suspected pulmonary embolism?

Answer 12

Check the WELLS Score

For a score > 4, do CTPA and give LMWH

For a score ≤ 4, do a D Dimer. If +ve for D Dimer, proceed to CTPA

If D Dimer -ve, consider alternative diagnosis

=> If there is a delay in arranging the scan, give a treatment dose of LMWH

Question 13

What are the categories of the Wells score?

Answer 13

FEATURE
Clinical signs and symptoms of DVT - 3
Heart rate > 100bpm - 1.5
Recently bed ridden - 1.5
Previous PE or DVT - 1.5
Haemoptysis - 1
Cancer receiving active treatment - 1
Alternative diagnosis less likely than PE - 3

SCORE GREATER THAN 4 MEANS LIKELY PE

Question 14

What is the management of PE?

Answer 14

• LMWH/Fondaparinux should be given immediately after diagnosis
• Warfarin given with 24 hours
• LMWH/Fondaparinux given for at least 5 days or until INR > 2.0 for at least 24 hours
• Warfarin given for 3 months, at 3 months risks and benefits of treatment are assessed
• Warfarin extended in unprovoked cases (NO RISK FACTORS)
• In patients with active cancer, LMWH used for 6 months

Question 15

How does PE present on an ECG?

Answer 15

Sinus Tachycardia or S1Q3T3

Question 16

What are the risk factors of PE?

Answer 16

• Recent surgery
• Thrombophilia
• Leg fracture
• Prolonged bed rest
• Malignancy
• Pregnancy or on pill
• Previous PE

Question 17

What is the WELLS score for PE?

Answer 17

Clinical features of DVT - 3 
Tachycardia - 1.5
Recent bed rest - 1.5
Previous DVT or PE - 1.5
Haemoptysis - 1 
Active cancer - 1
Alternative diagnoses are less likely than PE - 3