Pulmonary Embolism Flashcards

1
Q

Define PE

A

Obstruction of one or more pulmonary arteries by a solid, liquid or gaseous mass

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2
Q

Epidemiology PE

A
  • Accounts for many deaths per year
  • Incidence increases with age
  • M > F
  • Deaths due to VT = 34% attributable to sudden fatal PE
  • Increasing incidence of PE
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3
Q

Broad categories of PE aetiologies

A
  • Deep vein thrombosis (most common)
  • Fat embolism
  • Air embolism
  • Amniotic fluid embolism
  • Tissue embolism
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4
Q

Risk factors for a DVT

A
  • Obesity
  • Hypomobility
  • Malignancy
  • Pregnancy
  • Dehydration
  • OCP
  • Previous DVT
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5
Q

When are fat embolisms most common

A

During major surgical interventions

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6
Q

Pathophysiology behind PE

A
  • Thrombus formation that embolises to pulmonary arteries via the IVC (rarely SVC)
  • Leads to a partial or complete blockage of the pulmonary arteries
  • Thrombi rarely develop de novo in the pulmonary vasculature
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7
Q

Problems associated with lung and arterial obstruction

A
  • Infarction and inflammation
  • Impaired gas exchange
  • Cardiac compromise
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8
Q

Describe what happens when infarction and inflammation result from PE

A
  • Occurs in lung and pleura
  • Pleuritic chest pain and haemoptysis
  • Surfactant dysfunction leads to atelectasis and decreased paO2
  • Leads to respiratory alkalosis and hypocapnia (as respiratory drive triggered)
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9
Q

Describe what happens with impaired gas exchange in PE

A
  • Ventilation-perfusion mismatch

- Arterial hypoxaemia

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10
Q

Describe what happens with cardiac compromise with PE

A
  • Elevated pulmonary artery pressure leads to right ventricular pressure overload
  • Forward failure
  • Decreased cardiac output
  • Hypotension and tachycardia
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11
Q

Clinical features of PE

A
  • Acute onset of symptoms
  • Often triggered by a specific event (waking up, exercise etc)
  • Dyspnoea
  • Tachypnoea
  • Sudden chest pain - worse on inspiration
  • Cough and haemoptysis
  • Dullness on percussion
  • Decreased breath sounds
  • Tachycardia
  • Hypotension
  • Jugular vein distension
  • Low-grade fever
  • Syncope/shock/circulatory collapse with major PE
  • Possible symptoms of DVT
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12
Q

DDx for PE

A
  • Unstable angina
  • NSTEMI/STEMI
  • CAP
  • CHF
  • Acute bronchitis
  • Acute exacerbation of COPD or asthma
  • Pericarditis
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13
Q

What does Wells criteria measure

A
  • Score in stable patients - access probability of PE

also a Wells criteria for DVT

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14
Q

7 components of Wells

A
  • Clinical signs of DVT
  • Alternative diagnosis less likely than a PE
  • Previous PE or DVT
  • HR >100bpm
  • Surgery or immobilisation within 4 weeks
  • Haemoptysis
  • Active malignancy (treating/palliative/diagnosed <6months ago)
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15
Q

Score for a high chance of PE

A

> 4

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16
Q

Score for a low change of PE

A

<=4

17
Q

If patient is haemodynamically stable (SBP >90) and at high risk of PE, what is initial management on presentation

A
  • CTA/CTPA

- If contraindicated - immediate anticoagulant - unfractionated heparin

18
Q

If a patient is too unstable for CTA - what is first line management

A
  • Bedside echocardiogram - look for RV enlargement and visualise clot)
  • Done prior to empiric thrombolysis
19
Q

Management in someone at low probability of PE

A
  • Measure D-dimer, ABG and CXR
20
Q

Positive D-dimer

A
  • Not diagnostic for PE

- Progress to CTA

21
Q

Negative D-dimer

A
  • High probability no PE

- DDx

22
Q

What is the D-dimer test

A
  • D-dimers are fibrin degradation products detected in the blood after thrombus resolution via fibrinolysis
23
Q

Normal D-dimer level

A

<500ng/mL

24
Q

D-dimer test has high…..

A

Sensitivity and NPV = negative test can rule our PE

25
Q

D-dimer test has low….

A

Specificity = poor confirmatory test

26
Q

ABG and PE

A

Respiratory acidosis - decreased pO2, pCO2 and increased pH

27
Q

What is a CTPA

A

CT pulmonary angiogram - contrast enhanced imaging of pulmonary arteries

28
Q

Positives about CTPA

A
  • High sensitivity and specificity

- Visible intraluminal filling defects

29
Q

Why is a CXR done on PE management

A
  • Rule OUT other cuases
  • Check for atelectasis
  • Signs of PE on a CXR are rare
30
Q

Why is an echo done on PE management

A
  • Detect RA pressure signs
31
Q

Why is a VQ test done on PE management

A
  • Use as an alternative to CTPA in patients with severe renal insufficiency or contrast allergy
32
Q

Acute general treatment for suspected PE

A
  • Seated at 45 degrees
  • O2 supplementation and intubation
  • IV fluids and and vasopressors if hypotensive
  • Analgesics
33
Q

PE and empiric anticoagulation - contraindication

A

Bleeding risk

34
Q

Empiric anticoagulation - 0-10 days

A
  • LMWH (use unfractionated if renally compromised)
35
Q

Empiric anticoagulation - 3-6 months

A
  • Long term treatment and prophylaxis

- Warfarin, LMWH, direct oral anticoagulants

36
Q

Recanalisation and PE

A
  • Thrombolytic therapy = massive PE or haemodynamically unstable = use tPA (fibrinolysis)
  • Embolectomy = last resort = surgical or catheter based thrombus removal
37
Q

Interventional surgery prevention for PE

A

IVC filter

- Mechanical device implanted into IVC

38
Q

Medication prevention of PE

A

DVT prophylaxis

39
Q

PE complications

A
  • High risk of recurrence without treatment (5-10%)
  • RV failure
  • Atelectasis (20%)
  • Pulmonary effusion
  • Pulmonary infarction (10%)
  • Pneumonia (from infarction)