Respiratory: PE Flashcards

1
Q

Describe the primary factors that contribute to a thrombus formation [3]

A

Virchows triad:

Endothelial damage:
- Alters blood flow dynamics: creates turbulence and increasing flow friction within a vessel

Hypercoagulable state:

Blood stasis

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2
Q

State risk factors for PE

A

Increasing age
DVT diagnosis / previous VTE event
Surgery within last 2 months
Bed rest > 5 days
Fx of VTE
Active malignancy
Recent trauma
Pregnancy / post-natal period
Smoking
Obesity
Factor V Leiden mutation
Antithrombin deficiency
Prothrombin deficiency
Protein C & S deficiencies
Antiphospholiipid syndrome

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3
Q

Which inherited disorders increase the risk of PE? [5]

A

Factor V Leiden mutation:
- Normally used for blood clotting: helps enzyme reaction to form fibrin in blood clot
- Once the coagulation process is turned on in people with factor V Leiden, it turns off more slowly than in people with normal factor V

Antithrombin deficiency
- Normally anti-thrombin acts as the inhibitory component to thrombin formation

Prothrombin deficiency

Protein C & S deficiencies

Antiphospholiipid syndrome

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4
Q

Which type of hormone therapy increases the risk of PE? [1]

A

Hormone therapy with oestrogen (e.g., combined oral contraceptive pill or hormone replacement therapy)

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5
Q

Describe the presentation of PE

A

dyspnoea
- most common symptom
- can be acute or severe
- tachopynea is common in acute PE

chest pain:
- acute onset
- localised to one side of the chest (unlikely to be central!)

signs of concurrent deep vein thrombosis (DVT):
- Typically pain and swelling in one leg, although both legs may be affected

hypoxaemia:
- Oxygen saturations < 94% (or < 88% in patients at risk of hypercapnic respiratory failure).

failure to meet Pulmonary Embolism Rule-out Criteria (the PERC rule)

Cough

Haemopytsis

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6
Q

What is important to note about symptoms of dysopnea in PE? [1]

A

Symptoms of PE usually come on acutely rather than gradually.

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7
Q

Explain what is meant by the PERC rule

A

The pulmonary embolism rule-out criteria (PERC) are recommended by the NICE guidelines (2020) when the clinician estimates less than a 15% probability of a pulmonary embolism to decide whether further investigations for a PE are needed. If all the criteria are met, further investigations for a PE are not required.

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8
Q

Which factors make up the PERC rule? [8]

A

Age < 50 years

Heart rate < 100 bpm

SaO 2 on room air ≥95%

No unilateral leg swelling

No haemoptysis

No recent surgery or trauma (≤4 weeks ago requiring treatment with general anaesthesia)

No prior PE or DVT

No hormone use (oral contraceptives, hormone replacement, or oestrogenic hormones used in male or female patients).

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9
Q

What is next step if a patient fails the PERC test? [1]

A

Request D-dimer testing for any patient in whom the PERC rule fails to rule out a PE (i.e., one or more criteria not fulfilled)

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10
Q

What Well’s score indicates likelihood of PE? [1]

How do you use the Wells score to create a management plan for PE? [2]

A

> 4: PE likely
< 4: PE unlikely

Plan:
Likely: perform a CT pulmonary angiogram (CTPA) or alternative imaging
Unlikely: perform a d-dimer, and if positive, perform a CTPA

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11
Q

Describe the investigations you would conduct for a ptx suspected with PE

A

computed tomographic pulmonary angiography (CTPA)
- preferred investigation for definitive confirmation of PE

echocardiography:
- presence of any signs of right ventricular (RV) dysfunction is sufficiently suggestive of PE to confirm the diagnosis and justify urgent reperfusion treatment
- used if CTPA not immediately available / contraindicated

D-dimer:
- Elevated
- Used if Wells Score < 4.

ECG:
- An ECG is not diagnostic of PE but can be useful to support the diagnosis of PE or rule out other causes.
- S1Q3T3 pattern

urea and electrolytes:
- guides CTPA use

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12
Q

Why might a CTPA be contraindicated for PE investigation? [2]

A

The contrast dye used in CTPA for the evaluation of PE may cause nephropathy.

Radiation from CT is considered to be a risk factor for certain cancers.

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13
Q

Explain a specific sign seen on echocardiogram that would indicate a PE [1]

A

60/60 sign :a combination of
- pulmonary acceleration time (PAT) less than 60 milliseconds
and
- tricuspid regurgitation (TR) jet gradient of less than 60 mmHg

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14
Q

What is the McConnell sign? [1]
What does it indicate? [1]

A

reduced contractility of the RV free wall compared with the RV apex

indicates PE

Typically this looks as if the apex of the RV is a trampoline bouncing up and down while the rest of the RV remains still

Ty

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15
Q

Why do you need to conduct coagulation studies when suspicious of PE / VTE? [2]

A

Order international normalised ratio (INR), prothrombin time (PT), and activated partial thromboplastin time (aPTT). These are needed to establish baseline values before starting anticoagulation.

Also aids decisions about the safety and choice of initial anticoagulation.

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16
Q

What ABG results would indicate PE? [1]

Explain your answer [1]

A

TOM TIP: Patients with a pulmonary embolism often have respiratory alkalosis on an ABG.

Hypoxia causes a raised respiratory rate.

Breathing fast means they “blow off” extra CO2.

A low CO2 means the blood becomes alkalotic.

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17
Q

What are the two causes of respiratory alkolosis in an ABG? [2]

How do you differentiate between them? [2]

A

PE
and
Hyperventilation syndrome.

Patients with PE will have a low pO2

Patients with hyperventilation syndrome will have a high pO2.

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18
Q

Describe an alternative imaging method for investigating PE than CTPA

A

V/Q scan:

  • radioactive isotopes and a gamma camera to compare ventilation with the perfusion of the lungs
  • First, the isotopes are inhaled to fill the lungs, and a picture is taken to demonstrate ventilation
  • Next, a contrast containing isotopes is injected, and a picture is taken to illustrate perfusion
  • The two images are compared
  • With a pulmonary embolism: there will be a deficit in perfusion as the thrombus blocks blood flow to the lung tissue
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19
Q

A V/Q scan is of limited use in patients with which co-morbidities? [3]

A

A V/Q scan is of limited use in patients with:
* significant underlying lung disease
* left ventricular failure
* congestive cardiac failure

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20
Q

When is a V/Q scan indicated for suspected PE? [3]

A

Patients with:
* renal impairment
* contrast allergy
* risk from radiation

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21
Q

Label A [1]

A

Saddle embolus

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22
Q

State 4 reasons that may cause V/Q mismatch [4]

A

old pulmonary embolisms
AV malformations
vasculitis
previous radiotherapy

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23
Q

Describe the treatment algorithm for patients who have initial PE suspected and are haemodynamically unstable AND OR are hypoxaemic [2]

A

Oxygen
- Give high-concentration oxygen if oxygen saturations are < 90%, targeting an initial oxygen saturation of 94% to 98%

Consider fluid resuscitation
- Give intravenous fluids if SBP is < 90 mmHg and the JVP is not elevated
- fluid challenge of ≤500 mL over 15-30 minutes

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24
Q

What is the leading cause of death for patients with massive PE? [1]

A

The leading cause of death in patients with high-risk (massive) PE is acute right ventricular (RV) failure with resulting hypotension.[65]

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25
Q

Describe the treatment algorithm for patients who have PE confirmed and are haemodynamically unstable [4]

A

First line:
- heparin: 10,000 units intravenously as a loading dose initially, followed by 18 units/kg/hour intravenous infusion

PLUS: thrombolysis: (involves injecting a fibrinolytic (breaks down fibrin) medication that rapidly dissolves clot)
- Alteplase or
- Streptokinase or
- Urokinase

PLUS:
- anticoagulation with unfractionated heparin (UFH) for several hours after the end of thrombolysis before: switching to apixaban or rivaroxaban; low molecular weight heparin (LMWH) is an alternative if these are unsuitable - this is preferable

CONSIDER: vasoactive drug if SBP < 90 mmHG after thrombolysis
- noradrenaline or
- dobutamine

-

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26
Q
A

-

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27
Q

Describe the treatment algorithm for patients who have PE confirmed and are haemodynamically stable [4]

A

First line: anticoagulation:
- apixaban or
- rivaroxaban

OR

  • UFH / LMWH / Fondaparinux lead AND warfarin
  • Target INR 2-3 then stop heparin
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28
Q

Describe the long term managment of PE for:

  • most people [4]
  • patients suffering from antiphospholipid syndrome [1]
  • pregnant people [1]
A

DOACs: most people
- apixaban
- rivaroxaban
- edoxaban
- dabigatran

Warfarin: for antiphospholipid syndrome patients

LMWH for pregnant people

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29
Q

How long would you continue treatment for patients:
- with a reversible cause [1]
- unprovoked PE [1]
- with cancer p1[

A

Treatment time:
* 3 months with a reversible cause (then review)

  • Beyond 3 months with unprovoked PE, recurrent VTE or an irreversible underlying cause (e.g., thrombophilia)
  • 3-6 months in active cancer (then review)
30
Q

All patients of PE should have anticoagulation for at least [] months

A

All patients of PE should have anticoagulation for at least 3 months

31
Q

State 4 acute complications of PE

A

Right ventricular failure:

Cardiogenic shock:

Arrhythmias

Respiratory failure

32
Q

Describe the clinical consequence of PE causing right ventricular failure [2]

A

Large or multiple emboli can cause acute right ventricular (RV) dilata hypertrophy strain, leading to RV dysfunction and failure.

This may result in systemic hypotension, shock, and even sudden cardiac death.

33
Q

Describe how massive PE causes hemodyanmic collapse [7]

A
34
Q

Describe how PE can cause cardiogenic shock [2]

A

Cardiogenic shock
- Severe PE may lead to decreased cardiac output, causing systemic hypotension, impaired end-organ perfusion, and ultimately cardiogenic shock.

35
Q

Which arrythmias can PE lead to [3]

A

Arrhythmias: PE can provoke supraventricular and ventricular arrhythmias, such as:
- atrial fibrillation
- ventricular tachycardia
- ventricular fibrillation

which can further compromise hemodynamics.

36
Q

Describe three subacute complications of PE

A

Infarction and lung necrosis
- PE can cause ischemic injury to the lung parenchyma, leading to pulmonary infarction, haemorrhage, or lung necrosis.

Pleural effusion:
- Inflammatory processes triggered by PE may cause pleural effusion, which may be exudative or hemorrhagic.

Pneumothorax:
- Rarely, PE-induced lung infarction may lead to pneumothorax due to the rupture of a bulla or necrotic lung tissue

37
Q

Describe a chronic complication of PE [1]

A

Chronic thromboembolic pulmonary hypertension (CTEPH):

  • CTEPH is a rare but serious complication characterized by unresolved thrombotic occlusions in the pulmonary arterial system, turning into fibrotic tissue leading to increased pulmonary vascular resistance, pulmonary hypertension, and eventually right heart failure.
38
Q

What is the most appropriate next step in the investigation of suspected pulmonary embolism if D-dimer negative?

A

Stop anticoagulation and consider an alternative diagnosis

39
Q

What is the most appropriate next step in the investigation of suspected pulmonary embolism if medium-high (> 15%) pre-test probability of PE? [1]

A

A 2-level PE Wells score should be performed:

Clinical probability simplified scores
PE likely - more than 4 points
PE unlikely - 4 points or less

40
Q

What is the most appropriate next step in the investigation of suspected pulmonary embolism if CTPA negative? [1]

A

Consider the possibility of DVT and arrange proximal leg vein ultrasound if suspected

41
Q

What is the best investigation for pulmonary embolism (history of CKD stage 4)? [1]

A

Ventilation-perfusion scan

42
Q

PE would cause change to axis deviation? [1]

A

Right axis deviation

43
Q

Describe if lung tissue becomes infarcted during a PE

A

May infarct if not perfused by PE. But oxygen continues to be supplied by the bronchial circulation and airways

44
Q

Describe how a patient presents when they are suffering from massive / multiple PE causing RV failure [3]

A

Hypotension
Syncope
Sudden death

45
Q

How long post-partum increases the risk of PE by 20%? [1]

A

6 weeks

46
Q

Which form of cancer causes the most amount of PEs? [1]

A

Brain cancer

47
Q

What is important to consider about haemoptysis and PE? [1]

A

haemoptysis may be delayed by 3 days or more of other symptoms / PE event

48
Q

Describe the chest pain experienced in PE [1]

A

Pleuritic: worse on inspiration, sudden and sharp pain

49
Q

Describe how acute right heart strain would present with massive PE [4]

A
  • Loud P2
  • Wide splitting of 2nd heart sound
  • Gallop rhythm
  • Triscuspid regurgitation
50
Q

What do you need to consider when doing ABG for PE? [1]

A

20% have normal Pa02

51
Q

State 3 respiratory and 4 CVS differential diagnoses for PE

A

Respiratory:
- Pneumothorax
- Pneumonia
- Acute exaerbation of resp disease

CV:
- MI
- Pericarditis
- Aortic dissection
- Cardiac tampondade

52
Q

Which patient populations do you admit immediately if you suspect PE? [2]

A

Haemodynamically unstable
Pregnant / puerperium (6 weeks post)

53
Q

How do you determine if need to admit a patient with PE if they are haemodynamically stable and not pregnant?

A

Conduct a 2 Level Wells score:

If score >4: PE is likely
- Admit
- CTPA
- Interim therapeutic anticoagulation

If score < 4: PE is unlikely
- Conduct a D-dimer:
- Positive: admit, Interim therapeutic anticoagulation CTPA
- Negative: Consider alternative diagnosis

54
Q

How should you investigate using imaging for massive PE? [3]

A

Within 1hr
CTPA if safe
Beside echo can be diagnostic instead: shows RV failure

55
Q

What does this CT image depict? [2]

A

On the side: wedge shaped infarct where the lung is not being perfused

Arrow: big blood clot

56
Q

What is Westermark’s sign? [2]
What type of imaging does this sign occur in? [1]

A

Westermark’s sign:
- CXR
- Left mid / upper zone regional lucency (as the area is not perfused) with truncation of normal-left side pulmonary markings. Bilateral pleural effusions

Westermark sign is a chest x-ray finding of oligaemia (clarified area) distal to a large vessel that is occluded by a pulmonary embolus.

57
Q

What is Hampton’s hump? [1]

Be aware, don’t need to know

A

Wedge shaped infarct

58
Q

What ECG findings would a PE cause? [6]

A

Sinus tachycardia
New onset AF
Right axis deviation
RBBB
T wave inversion
P pulmonale
S1Q3T3

59
Q

Describe the S1Q3T3 ECG changes in PE [3]

A

deep S wave in lead I
Q wave in III
inverted T wave in III (20%)

60
Q

Under what conditions is a V/Q / isotope scanning suitable? [2]

A

Normal CXR
NO concurrent CVD

61
Q

How do you interpret a V/Q scan to indicate PE is occurring? [1]

A

Ventilation is normal / equal

Perfusion of lung: mismatched

62
Q

How do you alter imaging for PE investigations if patient is pregnant? [3]

A

Do half dose V/Q: lower risk for breast cancer (when pregnany, increased risk from radiation) BUT higher risk of childhood cancer

Just do perfusion imaging

Use CXR with lead protection for foetus

CTPA is more definitive

63
Q

Which drug is contraindicated in pregnancy, but safe with breastfeeding? [1]

A

Warfarin

64
Q

State 4 invasive procedures used to treat PE if needed

A
  • Embolectomy
  • Mechanical fragmentation with R heart angiography
  • Pulmonary thombro-endarterectomy
  • IVC filter
65
Q

Which of the following is used to treat chronic PEs unresolved after 3 months

  • Embolectomy
  • Mechanical fragmentation with R heart angiography
  • Pulmonary thombro-endarterectomy
  • IVC filter
A

Pulmonary thombro-endarterectomy (PTE)

66
Q

Name a risk [1] and benefits [2] of using unfractionated heparin in treating PE [4]

A

Risks:
- Heparin induced thrombocytopenia (HIT)

Benefits:
- Rapid reversal possible
- More rapid anticoagulation

67
Q

What is an IVC filter? [1]

When is it used? [3]

A

Traps fragmented thrombemboli on the way to pulmonary circulation

Used if:
- patient is contraindicated to anticoagulation in proximal PE/DVT
- Recurrent VTE despite anticoagulation tx
- Only temporary

68
Q

What level of thrombophilia should make sure that you screen a patient? [2]

A

< 50 & recurrent unprovoked VTE or strong FHx

69
Q

What ECHO findings might you find in acute PE? [6]

A

 Direct visualization of
thromboemboli in the RT heart
and PA.
 RV dilatation.
 RV dysfunction.
 Normal or hyper dynamic LV.
 Septal flattening.
 PA dilatation

70
Q

Describe the different bridging times for LMWH if using:
- Warfarin
- Dabigatran or edoxaban
- Rivaroxaban or apixaban

A

Warfarin:
- Start LMWH and initiate warfarin at same time then after 5-10 days change to just warfarin

Dabigatran or edoxaban
- 5 days of LMWH with both then switch to doac same day

Rivaroxaban or apixaban
- No bridge - only use them