PE Flashcards

1
Q

What is a pulmonary embolism?

A

Pulmonary embolism (PE) comprises “stuff” that enters the venous system and ends up in pulmonary circulation
• Vessels (venous) get bigger back to the heart
• Vessels (arterial) get smaller into pulmonary tree
• Blockage will occur at the level where vessel is too small to allow passage
• Pulmonary thromboembolism most common
• Venous thrombi often from lower extremities

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2
Q

Types of PE

A
  • Air (surgery, catheters)
  • Amniotic fluid (labour)
  • Fat (liposuction, long bone fractures)
  • Foreign body (talc, parts of IV devices)
  • Oil (lymphangiography)
  • Parasite eggs
  • Septic (endocarditis, thrombophlebitis
  • Tumour (renal cell with vena cava invasion)
  • Thrombus (DVT)
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3
Q

Risk factors for PE

A
Venous stasis:
• Bed rest
• Immobilasation (surgery, flights, drive)
• Low cardiac output (athletes)
• Pregnancy
• Obesity
• Hyperviscosity
• Vascular damage
• Central venous catheter
• Age (older)
• IV drug use
Coagulation:
• Tissue injury (infarction, surgery, trauma)
• Malignancy
• Lupus anticoagulant
• Nephrotic syndrome
• Oral contraceptive pill (oestrogen)
• Genetic coagulation disorders
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4
Q

Pathophysiology

A
  • Lower extremity DVT: 40-50% cases asymptomatic
  • DVT Symptoms – swelling, pain, tenderness

Normal leg:
Blood flows to the heart and the lungs

DVT:
Swelling and inflammation below the blockage site (venous clot)

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5
Q

DVT stages

A

Acute: Fresh coagulum, poorly attached to vein wall, risk of pulmonary embolisation, inflammation

Subacute: >7-14 days. inflammation diminishes or resolved, thrombus retraction and adherence to wall, variable lysis over weeks to months.

Chronic: Thrombus lyses or becomes fibrous scar. Possible debilitating venous stasis

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6
Q

Haemodynamic changes

A
  • Effect of obstruction depends on % of pulmonary circulation obstructed and any pre-existing cardiopulmonary disease.
  • Pulmonary artery pressure increases proportionally to the % of pulmonary circulation occluded.
  • Can cause right ventricular strain.
  • Sudden occlusion of pulmonary outflow will reduce cardiac output to zero = death.
  • Increased pulmonary vascular resistence can cause right ventricle strain and fatal decrease in cardiac output.
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7
Q

Ventilation and perfusion

A
  • PE reduces perfusion distal to occlusion.
  • This causes increased alveolar dead space.
  • This impairs excretion of carbon dioxide.
  • Leads to hyperventilation.
  • Eventually (hours) this leads to alveolar oedema, alveolar collapse and atelectasis.
  • The end result is arterial hypoxaemia.
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8
Q

Hypoxaemia

A
  • Mild to moderate hypoxaemia is the most common finding in PE
  • That manifests as low PaCO2
  • Can also result from right to left shunting
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9
Q

Signs and symptoms of PE

A
Classic triad:
• Sudden onset dyspnoea (73%)
• Pleuritic chest pain (44-66%)
• Haemoptysis (13%)
• Cough (37%)
Evidence of DVT most compelling sign, calf:
• Swollen • Tender • Warm
• Red
Other:
• Tachypnoea
• Cyanosis (blue lips) • Fever
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10
Q

ECG changes in PE

A

75% of ECGs will be abnormal in PE

Non specific
• Sinus tachycardia
• T wave inversion on precordial leads
• ST and T wave changes
• Deep S wave on lead I, Q wave and inverted T wave on lead III due to right ventricular strain
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11
Q

DVT ultrasound

A
  • Sensitivity 97% proximal lower limb
  • 73% for calf
  • Fail to compress (best sign)
  • Markedly distended vein
  • Thrombus hypoechoic, homogenous
  • Small flow streams around and through thrombus (tram track)
  • Free floating thrombus (unattached proximal end)
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12
Q

DVT CT Venography

A
  • Filling defect in lumen
  • Collateral veins
  • Perivenous inflammation
  • May see compressing mass along veins eg. pelvis
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13
Q

CXR pulmonary embolism

A
  • CXR nonspecific
  • 10-12% normal
  • Enlarged central pulmonary artery (knuckle sign), commonly right interlobar pulmonary artery due to physical presence of clot
  • Focal oligemia (Westermark sign) due to vascular obstruction
  • Necessary to exclude other lung disease
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14
Q

CTPA pulmonary embolism

A

CTPA
• Sensitivity and specificity = 90%
• Negative CT angiograms – risk of missed fatal embolism 0-
0.7%

Indications:
• Clinical suspicion of PE
• Cardiac or lung disease excludes VQ scan
• Indeterminate VQ scan
• Chest xray not clear to indicate VQ useful
• Pulmonary hypertension
• Immediate diagnosis needed (USA protocol for ventilation)

Findings typically either:
• a filling defect within the pulmonary artery • abrupt cut-off of artery
• the latter is definitive
• the former, particularly if small vessels, lacks haemodynamic status / significance

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15
Q

Limitations of CTPA

A
  • Radiation dose (2.0 rad to EACH breast) • Patient motion
  • Morbid obesity
  • Contrast bolus timing
  • 20% of CTPA below quality standard • True haemodynamic significance?
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16
Q

VQ lung scan

A
  • Ventilation (USA versus Aust protocol)
  • Perfusion
  • Mismatch
  • PE = peripheral, wedge shaped, segmental or sub segmental perfusion defects (hypoperfusion) in the absence of a ventilation defect (mismatch)
17
Q

Treatment for PE

A
  • Anticoagulants are first line therapy.
  • They stop blood clots from getting bigger and prevent new clots forming.
  • They do not break up blood clots that have already formed.
  • PE sufferers may be on anti-coagulants for 3-6 months; longer with prior PE history.
  • Reduces mortality from 30 to 10%.
  • Low molecular weight heparin in acute phase
  • Oral warfarin longer term.
  • Cease heparin after INR (international normalised ratio) hits 2.0 (not before 5 days)

If PE is life threatening, thrombolytics may be
used to break down clots.
• Bleeding risk.
• A catheter may also be used.
• Embolectomy is uncommon but may be an option
• Vena cava filter