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Cardiology > Pulmonary Embolism > Flashcards

Pulmonary Embolism Flashcards

1
Q

What is a pulmonary embolism?

A

https://www.youtube.com/watch?v=Lp65yGitCNo

A venous thrombi, usually from a DVT, passes into the pulmonary ciruclation and blocks flow to the lungs

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2
Q

What are risk factors for PE?

A
  • Trauma
  • Hormones - COCP, pregnancy
  • Road traffic accidents
  • Operations
  • Malignancy
  • Blood disorder - polycythaemia etc.
  • Old age, obesity
  • Serious illness
  • Immobilisation
  • Splenectomy

Others include dehydration and previous DVT

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3
Q

What symptoms might you see in someone with a PE?

A

Sudden onset

  • Dyspnoea - can be severe, and worsened by exertion
  • Cough +/- haemoptysis
  • Pleuritic chest pain
  • Syncope
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4
Q

What is the mechanism behind dyspnoea in thromboembolism?

A

It is thought that pressure receptors or C-fibres in the pulmonary vasculature or right atrium are activated and interact with central systems, contributing to dyspnoea

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5
Q

Why can haemoptysis occur in PE?

A

Any condition that results in pulmonary venous hypertension may cause haemoptysis. For example, left ventricular failure can lead to increasingly high pulmonary venous pressures. These high pressures damage venous walls, causing blood excursion into the lung and eventually haemoptysis.

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6
Q

Why might you get raised JVP in PE?

A

PE may be large enough to create back pressure into the right heart, atrium and venous system, thus resulting in

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7
Q

In a PE, which physiological process occurs (alveolar dead space or shunting) and what would be the V/Q ratio (>1)?

A

Alveolar dead space - V/Q mismatch >1

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8
Q

Why does tachycardia occur in PE?

A

Activation of the sympathetic nervous system and/or catecholamine release due to a combination of hypoxia and reduced stroke volume and resultant CO (heart tries to compensate)

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9
Q

Why can those with PE develop a gallop rhythm?

A

Due to heart failure caused by PE - rapid ventricular against stiff ventricular walls causes the sound

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10
Q

Why would you get a loud P2 in PE?

A

Increased PHT of any cause causes the pulmonary valve to slam shutand cause a louder than normal P2

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11
Q

Why would you get right ventricular heave in PE?

A

RHF

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12
Q

Why might you get a pleural rub in PE?

A

Inflammatory process is triggered by emboli, which spreads into the plerua and causes loss of normal pleural lubrication

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13
Q

What causes tachypnoea in PE?

A

Compensatory response to either a drop in O2 or a rise in CO2

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14
Q

Why might you get central cyanosis in someone with PE?

A

A V/Q mismatch or shunting of blood through the lungs, without adequate oxygenation, will increase the quantity of deoxygenated haemoglobin that passes out of the lungs, leading to reduced oxygen saturation

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15
Q

What signs might you see in someone with a a mild PE?

A
  • Tachycardia
  • Tachypnoea
  • Calf swelling, erythema, oedema, tenderness
  • Decreased SpO2
  • Pleural Rub
  • Decreased breath sounds
  • Mild fever
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16
Q

How would you approach investigating someone with a PE?

A

Decide if non-massive or massive. If non-massive - Wells score, then:

  • Confirm diagnosis
  • Determine severity
  • Look for causes
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17
Q

How would you confirm/Exclude the diagnosis of PE?

A
  • Low Wells score - D-Dimer - if negative exclude
  • High Wells score or D-dimer positive - CTPA or V/Q (if CTPA contraindicated)
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18
Q

What investigations would you do when trying to determine the severity of a PE/the effect that it has had?

A
  • Clinical Signs
  • Bloods - ABG’s, FBC, U+E’s
  • ECG
  • CXR
  • CTPA
  • Echocardiogram
  • Bilateral leg Doppler (look for DVTs)
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19
Q

What might you see on ECG in someone with a PE?

A
  • Sinus Tachycardia
  • RV strain - T-wave inversion V1 to V4 and inferior leads, RBBB, right axis deviation
  • RA enlargement - P pulmonale, RV dilation i.e. dominant R in V1
  • S1Q3T3 pattern - rare
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20
Q

What might you see on X-ray in PE?

A
  • Hampton Hump - Wedge infarcts
  • Westermarks signs - Regional oligaemia
  • Fleischer’s Sign - Enlarged pulmonary artery
  • Elevated hemidiaphragm
  • Effusions
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21
Q

What are the criteria for the PE Wells Score?

A
  • Clinical signs and symptoms of DVT = +3
  • Alternative diagnosis less likely = +3
  • HR >100 = +1.5
  • Immobilisation (>3/7days) / surgery in the past month = +1.5
  • Previous DVT/PE = +1.5
  • Haemoptysis = +1
  • Cancer - on treatment, past 6 months or palliative = +1
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22
Q

What signs might you see in someone with a severe PE?

A
  • Decreased SpO2
  • Tachycardia
  • Tachypnoea
  • Hypotension
  • Raised JVP with prominent a wave
  • Gallop rhythm
  • Pleural rub
  • Loud P2 and splitting of S2
  • Tricuspid/pulmonary regurgitation
  • Right venticular heave
  • Cyanosis
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23
Q

If you suspected a massive PE, how would you investigate?

A

CTPA or Bedside Echo

Move to HDU

24
Q

What would you do if someone with a suspected non-massive PE had a Wells score <2 (low probability)?

A
  1. Assess based on PE ruke out criteria - If all criteria met PE Excluded
  2. If Unsure - Do D-dimer
  3. If D dimer > 500 ng/mL -> CTPA
25
Q

What would you do if someone with a suspected non-massive PE had a Wells score of 2-6 (intermediate risk)?

A
  • Measure D-Dimer - If > 500 ng/mL -> CTPA
  • If not feasible/inconclusive -> VQ scan
26
Q

What investigations might you do to look for the causes of PE?

A
  • USS - Legs, abdo and pelvis
  • CT - Abdo/pelvis
  • Inherited coagulopathy screen
  • Autoimmune screen
27
Q

What is the gold standard investigation for PE?

A

CT pulmonary angiography

28
Q

When would you start LMWH in someone with a suspected PE?

A
  • High risk - start before CTPA
  • Medium risk - if CTPA cannot be done within 4 hours
  • Low risk - if CTPA cannot be done within 24 hours
29
Q

When would you start warfarin in someone with a suspected PE?

A

After PE has been confirmed

30
Q

What dose of LMWH would you start someone on with a suspected PE?

31
Q

How would you immediately manage someone with a PE who was haemodynamically stable?

A
  • O2 therapy
  • IV cannulation
  • LMWH (when suspected), then switch to warfarin (when confirmed)
  • Analgesia
  • IV fluids - if hypotensive
  • Consider thrombolysis
32
Q

When would you consider thormbolysis in someone with a PE?

A
  • Haemodynamic instability - systemic hypotension, Evidence of RHF
  • Cardiac arrest
33
Q

What thrombolytic agents could you use for a PE?

A
  • Alteplase
  • Streptokinase
34
Q

Why do you need to be careful when giving opiods in PE?

A

Can cause systemic vasodilation, worsening hypotension

35
Q

What other options are available in those who thrombolysis is contraindicated in?

A
  • Pulmonary embolectomy
  • IVC filter
36
Q

Why do those with PE become hypoxaemic and hypocapnic on ABG?

A

https://www.youtube.com/watch?v=CfjGhwQiDOE

A PE causes V/Q mismatch and inflammation. Inflammation causes bronchoconstriction which causes hypoxia, leading to respiratory centres increasing respiratory drive, cause CO2 to be blown off

37
Q

What would you see on ABG in someone with PE; acidosis or alkalosis?

A

Respiratory alkalosis

38
Q

What is D-Dimer?

A

A fibrin degradation product (or FDP), a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis. It is so named because it contains two D fragments of the fibrin protein joined by a cross-link.

39
Q

Why would you not give diuretics orr vasodilators in PE?

A

Will cause worsening hypotension due to reduction in cardiac output and reduced TPR

40
Q

Why do you give LMWH cover whilst starting somone on warfarin?

A

Warfarin initially decreases protein C levels faster than the coagulation factors, it can paradoxically increase the blood’s tendency to coagulate when treatment is first begun (many patients when starting on warfarin are given heparin in parallel to combat this), leading to massive thrombosis with skin necrosis and gangrene of limbs. Therefore heparin is used to cover this hypercoagulable state

41
Q

What additional investigations woul you consider in women over 40 with unprovoked DVT?

A
  • CT Abdo/Pelvis
  • Mammogram
42
Q

Why does impaired gas exchange occur in PE?

A

Due to mechanical and functional obstruction of vascular bed altering V:Q ratio, and also due to inflammation resulting in surfactant dysfunction and atelectasis causing intrapulmonary shunting

43
Q

How common is hypercapnia and acidosis in PE?

A

Uncommon - unless someone is shocked due to massive PE

44
Q

Why can hypotension occur in PE?

A

Diminished SV and cardiac ouput due to PE obstructing pulmonary vascular flow, combined with hypoxic vasoconstriction.

Right ventricle also becomes backed up and dilated; combination of all of these factors results in a reduction in LV preload and thus CO.

45
Q

What would you do if someone with a suspected non-massive PE had a Wells score of >6 (high risk)?

A
  • Straight to CTPA
  • If inconclusive/unfeasible - V/Q scan
46
Q

Why might you consider doing a CXR in someone with features of a PE?

A

To exclude other causes of the symptoms - pneumonia, pleurisy, empyema

47
Q

How would you define someone with a PE as haemodynamically unstable?

A

PE presenting with hypotension

  • SBP <90 mmHg for a period >15 minutes
  • Hypotension requiring vasopressors
  • Clear evidence of shock
48
Q

How would you approach managing someone who was haemodynamically stable with PE?

A
  1. Assess whether anticoagulation is contraindicated
  2. Determine clinical suspicion of PE - Anticoagulate based on this
  3. Diagnostic evaluation - once anticoagulated
  4. Determine if clinical severity warrants thrombolysis
    • If yes -> thrombolyse
    • If no -> continue anticoagulation
49
Q

What Oral factor Xa inhibitors can be used to treat PE?

A
  • Rivaroxiban
  • Apixaban
  • Dabigatran
  • Edoxaban
50
Q

What would you consider giving someone you had started on edoxoban or dabigatran in someone with a PE?

A

LMWH for 5 days initially

51
Q

What is regarded as the first choice anticoagulant for treating PE?

A

Rivaroxiban

52
Q

What is regarded as the second choice medical treatment for PE?

A

LMWH followed by warfarin therapy

53
Q

What is the minimum amount of time that someone with a PE should be on anticoagulation?

54
Q

How long should someone with unprovoked PE be on anticoagulation?

A

6-12 months

55
Q

What might you want to investigate for in individuals with unprovoked PE before stopping anticoagulants?

A
  • Antiphospholipid syndrome
  • If 1st-deg FH of DVT/PE - Hereditary Thrombophilia screening

Cardiology (29 decks)

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