Pulmonary Embolism Flashcards

1
Q

What is pulmonary embolism?

A

When a thrombus, usually from a deep vein in the leg, embolisms/breaks away and travels through the bloodstream and dislodges in a pulmonary artery in the lungs, blocking it.

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2
Q

What is Virchow Triad?

A
  • Change in blood constituents- hypercoaguabolity
  • Change in pattern of blood flow- abnormal blood flow
  • Change in blood vessels wall- abnormal vessel wall
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3
Q

what does virchows triad do?

A

Promotes thrombus formation

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4
Q

What are the symptoms of pulmonary embolism?

A
  • pleuritic chest pain
  • haeompytsis
  • symptoms of deep vein thrombosis- stiffness and pain in leg
  • tachycardia
  • hypotension
  • dyspnoea
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5
Q

What are risk factors for Pulmonary embolism?

A
  • recent surgery- specifically abdominal/pelvic
  • Cardiorespiratory problems e.g. COPD
  • congestive heart failure
  • Varicose veins
  • Fractures
  • Increasing age
  • Malignant disorders
  • Pregnant
  • Immobile
  • THROMBOTIC DISORDERS! main one.
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6
Q

Where do thrombotic disorders usually occur from?

A
  • deep veins
  • external iliac vein
  • femoral vein
  • deep femoral vein
  • popliteal vein
  • posterior tibial vein
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7
Q

Where do thrombotic disorders usually not occur from?

A
  • Great saphenous vein

- Right sided heart failure.

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8
Q

What is a thrombus made up off?

A

red blood cells, platelets, fibrin meshwork, lines of Zahn

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9
Q

Explain fibrin formation

A

X -> Xa -> Prothrombin 11 -> Thrombin 11a

Thrombin does
Fibrinogen-> Fibrin

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10
Q

What does plasmin do?

A

Plasmin binds to fibrin activated by tissue plasminogen activators.

Causes the release of D dimers frrom the Fibrin.

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11
Q

What are measurements of anticoagulant activity?

A
  • D dimer assay
  • PT (extrinsic pathway, common pathway)
  • APTT (intrinsic pathway, common pathway0
  • INR- international normalised ratio
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12
Q

What does APTT show?

A

Activated pro thrombin plasmin time.

  • measures IV heparin coagulation
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13
Q

What does PT show?

A
  • Pro thrombin time.
  • Effects of warfarin.
  • Warfarin affects the extrinsic pathway
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14
Q

What is higher INR what does its show?

A

2,3

  • Less coagulation i.e. you bleed more easily.
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15
Q

Describe the movement of the emboli

A

up the inferior vena cava to the heart, right atrium -> right ventricle -> pulmonary trunk-> specific pulmonary artery

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16
Q

Describe the pathophysiology of pulmonary embolism?

A

Leads to
1) Increase in pulmonary vascular pressure (causing the back flow of blood to right hand side of heart)

2) Increase in right ventricular pressure (dilates the right ventricle)
3) Right sided heart failure. (decreases stroke volume, decreases cardiac output, decreases blood pressure)

  • Whatever happens to right side -happens on left side of heart.
  • Decrease in CO detected by receptors stimulating the sympathetic response(vasoconstriction)
  • Hence the symptoms of tachycardia and hypotension(although trying to increase BP the pulmonary emboli is still in the artery regardless)
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17
Q

What is the effect of pulmonary embolism on the lungs?

A

Leads to

1a) Ventilation/Perfusion mismatch causing abnormal gas exchange.
1b) ) Inflammation, causing the release of cytokines, bronchoconstriction, decreases the amount of oxygen going in, stimulating hyperventilation.
- Hypocapnea and hyoxaemia

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18
Q

What is ventilation, what is perfusion?

A

Ventilation(V) is movement of air in and out of the lungs

Perfusion(Q) is blood flow in and out of the lungs

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19
Q

What is hypocapnea and hyperaemia known as?

A

Respiratory alkalosis

20
Q

How can we see respiratory alkalosis?

A

Arterial blood gas test

21
Q

What investigations are carried out for pulmonary embolisms?

A
  1. CXR
  2. ECG
  3. CT Pulmonary angiogram (gold standard.)
  4. V/Q scan (later steps)
  5. D Dimer assay
  6. Echocardiogram
22
Q

What is the gold standard investigation for pulmonary embolism?

A

CT pulmonary angiogram

23
Q

What does a CXR exclude?

A
  • excludes pneumothorax and pneumonia
24
Q

What does a CXR show In pulmonary embolisms?

A
  • elevated hemidiaphragm
  • wedge shaped opacity where infarction has occurred
  • enlarged pulmonary trunk
  • pleural effusion
25
Q

What does an ECG exclude?

A
  • Pericarditis and myocardial infarction
26
Q

What does an ECG show?

A
  • sinus tachycardia (shorter intervals between R-R)

- right ventricular strains in leads V1-V4 (T wave inversion)

27
Q

What is used to help establish if its a pulmonary embolism or not?

A
  • Wells criteria
28
Q

Outline the Wells criteria

A
  1. DVT symptoms 3
  2. Other non DVT symptoms 3
  3. Haemopytsis 1
  4. HR>100 bpm 1.5
  5. Immoblisation (>3days) or surgery in last 4 weeks 1.5
  6. Previous DVT 1.5
  7. Malignancy 1
29
Q

What is the grading to establish if PE or not in the wells criteria?

A

> 4 Likely to be more PE

<4 Less likely to be PE

30
Q

What are the next steps if for wells, it is less likely to be PE?

A

D Dimer assay, assesses coagulant activity.

31
Q

What are the next steps if for wells, it is more likely to be PE?

A

CT Pulmonary angiogram

32
Q

What is the D Dimer Assay?

A

Fibrin links together with its D segments in a crosslinking meshwork.

-Plasmin, attaches to fibrin breaking it own which causes the release of D dimers

33
Q

You’ve done Wells got unlikely done D dimer and got unlikely. What are the next steps

A

Most likely not PE

34
Q

You’ve done Wells got unlikely done D dimer and got likely. What are the next steps

A

ct Pulmonary angiogram

35
Q

What to do if ct pulmonary angiogram is not sure?

A

ventilation perfusion V/Q scan

36
Q

What to do if CT pulmonary angiogram is positive?

A

Treatment!
1. General i.e. oxygen and fluids, opiates for pain but we aware bc of hypotension

  1. Anticoagulation to prevent further blood clot i.e. IV Heparin, subcutaneous heparin and warfarin.
  2. Thrombolytic therapy to break down the forming blood clot i.e. teneceteplase
37
Q

What is the treatment? Describe in detail.

A
  1. General i.e. oxygen and fluids, opiates for pain but we aware bc of hypotension
  2. Anticoagulation to prevent further blood clotS. Minimum 3 months, sometimes lifetime depending on risk.
    a) IV Unfractioned
    b) LMWH (subcutaneous)
    c) Warfarin
  • Stop heparin, keep warfarin.
  • Warfarin takes 5 days to take effect, hence dual ac therapy.
    3. Thrombolytic therapy to break down the forming blood clot i.e. tenecteplase.
38
Q

What is thrombolytic therapy used for?

A

Acute massive pulmonary embolisms and shock

39
Q

how does heparin work?

A

Inhibits X-Xa
Prothrombin (11) -> thrombin (11a)
Preventing fibrin meshwork

40
Q

How does warfarin work?

A
  • Vitamin K antagonist.
  • blocks the synthesis of clotting factors II, VII, IX, X (2,7,9,10)
  • X- Xa
    Prothrombin (II)-> thrombin (IIa)
41
Q

What is the aim with warfarin?

A

INR>2 but below three.

42
Q

How to check warfarin?

A

INR, INR>2, below 3

43
Q

What does warfarin effect?

A

Extrinsic pathway hence use PT

44
Q

How to measure the effects of IV heparin?

A

APTT

45
Q

What is pathogenesis of thrombus?

A
  • Hypercoaguablity of blood
  • Endothelial injury
  • Turbulent blood flow