Lecture 8 - Pulmonary Embolism Flashcards

1
Q

What is an embolism?

A

A blockage/lodging of material inside a blood vessel

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2
Q

What are the different types of embolism?

A

Thrombus
Fat
Gas (air, nitrogen)
Amniotic fluid
Foreign material

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3
Q

What is the main cause of a fat embolus?

A

Bones break which allows the fat from the bone to leak into the blood

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4
Q

What is a Venous Thromboembolism (VTE)?

What is the most common cause of a Venous Thromboembolism?

A

Where an embolism is caused by a thrombus which had formed n the venous system

Most common cause is DVT (Deep Venous Thrombosis)

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5
Q

How can a DVT/Venous Thromboembolism cause a pulmonary embolism?

A

Thrombus from the the lower limb/systemic vein will travel via the vena cava (inferior) through the right side of the heart to the pulmonary arteries

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6
Q

What percentage of Pulmonary Embolisms are caused by lower limb DVTs?

A

90%

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7
Q

What is Virkoffs Triad?

A

The 3 groups of risk factors for development of a DVT/VTE which can then go onto cause a pulmonary embolism

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8
Q

What are the 3 categories of Virkoffs triad which can increase the risk of VTEs/DVTs and so pulmonary embolisms?

A

Haemdynamic changes/stasis or turbulence

Hyper coagulability

Vessel wall damage/dysfunction

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9
Q

What are some risk factors for development of a VTE/DVT and therefore a PE that fit in Virkoffs triad?

A

Immobility (stasis)
Long distance travel (stasis)

Hyper coagulability:
-malignancy (pancreatic, colon)

Obesity + Pregnancy (stasis + Hyper coagulability)

Surgery + injury (vessel wall damage)

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10
Q

What are the 3 main impacts of a Pulmonary Embolism?

A

Acute right sided heart strain

Respiratory failure

Pulmonary infarction

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11
Q

How can acute right sided heart strain/failure occur with a pulmonary embolism?

A

The PE blocks the pulmonary artery
Leads to Pulmonary artery pressure increasing
This leads to blood backing up into the right ventricle leading to it dilating/overstretching (right sided HF)

Since less blood going to systemic circulation/left side systemic blood pressure drops, this leads to the heart pumping harder to try and compensate further increasing the pressure of the pulmonary arteries

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12
Q

How can a PE embolism lead to cardiac arrhythmias leading to cardiac arrest?

A

The overstretching of the right ventricle wall due to the high pulmonary arterial pressure leads to death of cells in the right ventricle

This heart tissue replaced by fibrous scar tissue which doesn’t conduct the electrical signals

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13
Q

What are the dangers of acute right ventricular overload (due to the PE)?

A

The pressure in the right side of the heart massively increases

This can force open the closed fossa ovalis causing a patent Foramen Ovale

This causes right to left shunting of deoxygenated blood leading to severe hypoxia causing cyanosis

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14
Q

How can Respiratory failure occur due to a PE?

A

Much less blood being received by alveoli from pulmonary arteries (reduced perfusion)

V/Q mismatch

Q much lower so V/Q > 1

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15
Q

How can a PE cause a Pulmonary Infarction?

A

Small embolisms cause alveolar haemorrhages and infarction

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16
Q

What are some clinical signs of Pulmonary Infarction and therefore PE?

A

Haemoptysis (coughing blood)
Pleuritis
Pleural effusion (bleed into the costodiaphragmatic recess)

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17
Q

How can you see a Pulmonary infarction?

A

A CXR
Appears as a Hampton hump (which is a paler area of tissue which has died)

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18
Q

What are the symptoms of a Pulmonary embolism?

A

Dyspnoea (breathlessness)
Pleuritic chest pain
Diaphoresis (sweating)
Cough
Haemoptysis (coughing blood)
Syncope (fainting)
Unilateral leg pain/swelling (indicates the DVT/VTE)

19
Q

What are some signs of a PE?

A

High Respiratory Rate (RR>16/min) crackles/rales

High HR >100bpm. (Heart murmurs)

Signs of DVT:
-cyanosis
-diaphoresis (sweating)
-low grade fever (any higher than 39C is likely not a PE)

20
Q

What type of pain is pleuritic chest pain?

A

Sharp localised pain

21
Q

What are some potential differentials if a patient presents with chest pain?

A

Pneumothorax
Pneumonia
Myocardial Infarction (MI)
Pericarditis
Pleurisy
MSK chest pain

22
Q

What are the first line investigations if you suspect a PE?

A

ECG
CXR
Blood tests
CTPA

23
Q

Why is it important that an ECG is done in patients who you suspect have a PE?

A

To rule out a MI (shows chest pain has other explanation)

24
Q

What are the classic findings on an ECG in a patient with a PE?

A

SIQ3T3

Sinus tachycardia

Right Bundle Branch Block

25
Q

What is the S1Q3T3 presentation in an ECG with a PE?

A

Deep S wave in Lead 1
Pathological Q wave in Lead III
Inverted T wave in lead III

26
Q

What blood tests are done in a patient with suspected PE?

A

Areterial Blood Gas (ABG) PAO2 = low

FBC, U&E, cRP, troponin levels and D-Dimers

D-dimers is very important

27
Q

What are D-dimers?

A

Protein fragments which are the degradation product of fibrin which is a key protein in a blood clot

28
Q

If a patient has a VTE what should their D-DImer result be?

A

Positive/raised

29
Q

Does an elevated D-dimer mean that a patient definitely has a PE/VTE?

Describe its positive predictive value:

A

No D-dimers can be elevated for many reasons

Poor positive predictive value

30
Q

If a patient is low risk for a VTE and has a negative D-dimer does this rule out a PE?

A

Yes it does

31
Q

What score do you use to determine whether a patient is low or high risk for a PE?

A

Wells Score

32
Q

What Wells Score indicates that a patient is likely to develop a PE?

A

Score over 4

33
Q

What are the main imagings done when a PE is suspected?

A

CXR (always done first)

CTPA (CT Pulmonary Angiogram)

V/Q scan (not often done, only ever done if CTPA cant be done due to pregnancy or poor renal function since these make it unsafe to use contrast))

34
Q

How do you treat a PE?

A

O2

Then treat the clot
Anticoagulants
Thrombolytics
Mechanical removal (surgery)

35
Q

What anticoagulants are given to help treat a PE?

A

Warfarin
Heparin (Low Molecular Weight Heparin)
DOACs

36
Q

What is the function of anticoagulants in treating a PE?

A

Then don’t actually break down the clot they just prevent the clot propagating/forming more clots
This allows the body to lyses down the clot

37
Q

What is an example of a Low Molecular weight heparin?

A

Dalteparin

38
Q

What is the danger of given anticoagulants like Heparin?

A

Patient may end up forming many clots

Called Heparin Induced Thrombocytopenia (HIT)

39
Q

What is the danger of Heparin-Induced Thrombocytopenia?

A

Many platelets activate forming many thrombi which propagate which can lead to stroke, MI and limb ischamiea

40
Q

If HIT starts to occur how to you treat the PE?

A

Change to a different anticoagulant that’s not Heparin

41
Q

What is oesophageal Varices?

What causes it?

A

Big Distended arteries in the oesophagus

Caused by alcohol consumption

42
Q

When might you have to be careful giving patients anticoagulants?

A

People with high bleeding risk:

-oesophageal Varices
-previous Haemorrhagic stroke
-severe thrombocytopenia

43
Q

What preventative methods can be employed to prevent a PE (Virkoffs triad)?

A

Anticoagulants
Anti Embolic Stockings/socks
Intermittent pneumatic compression
Falls prevention and avoid unnecessary invasive procedures (vessel wall damage)

44
Q

What is the first line treatment for a PE?

A

Low Molecular Weight Heparin (anticoagulant)