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Respiratory > Lecture 12- Pulmonary embolism > Flashcards

Lecture 12- Pulmonary embolism Flashcards

1
Q

Embolism

A

Obstruction of blood vessel by a foreign substance or blood clot that travels through the bloodstream, lodging in a blood vessel, plugging the vessel

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2
Q
  • Material may or may not derived from the
A
  • circulation itself
    • Clots from artery (heart arrack) or venous (PE)
      • thrombus
    • Air
    • Tumour
    • Fat- e.g. motor vehicle accident when bone marrow can go into circulation if bone crushed
    • Amniotic fluid
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3
Q
  • Pulmonary embolism means that the material passes through the
A
  • right side of the heart and lodges in the pulmonary arteries
    • Can be smaller branches
    • Could be main pulmonary trunk deadly
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4
Q

Angiogram showing the right pulmonary artery

A
  • Loss of vasculature due to embolism stopping significant blood flow to the lung
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5
Q
  • 90% of PE arise from
A

DVTs in legs, particularly popliteal vein and more proximal veins including pelvic veins

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6
Q
  • only …..% of patients with PE have symptoms or signs of DVT
A

25%

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7
Q

upper extremity clots are formed by

A

‘lines’ e.g. used to give chemotherapy, forming clots which pass through the venous system

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8
Q

PE stats

A
  • 3rd cause of vascular death after MI and stroke
  • Commonest cause of preventable death in hospital
  • One of the commonest cause of unexpected death in hospital pts
  • Risk factors same for DVT
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9
Q

risk factors for PE

A

virchows triad

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10
Q
  • Virchow’s triad
A
  • Endothelial injury
  • Statis of blood flow
  • Hypercoagulability
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11
Q
  • Endothelial injury
A

e.g. Hip fracture damages blood vessels

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12
Q
  • Statis or turbulence of blood flow
A
  • E.g long haul flight
  • E.g. immobility – fractured hip
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13
Q
  • Blood hypercoagulability
A

e.g.

  • Cancer
  • COCP
  • pregnancy
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14
Q

Pathology of deep venous thrombosis

A
  1. Changes in blood composition, reduced blood flow and changes to vessels can result in the formation of fibrous clots
  2. Clots form through activation of the coagulation cascade
  3. if clots form in legs= DVT
  4. If part of the clot goes to the lungs = PE
  5. Anticoagulants guideline treatment
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15
Q

coagulation cascade

A

fibrinogen –> fibrin –> fibrin mesh –> insoluble

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16
Q

full coagulation cascade

A
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17
Q

risk factors for thromboembolism

A
  • pregnancy X6
  • prolonged immobolisation x3
  • previous VTE x3
  • contraceptive pill x3
  • long haeul travel x3
  • cancer
  • heart failure
  • obesity
  • surgery >30 mins
  • HRT
  • thrombophilia

ALLL MAKES YOU HYPERCOAGULABLE

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18
Q

Presence of risk factors in patients with PE

A
  • 50% have an identifiable temporary risk factor
    • Surgery
    • Oestrogen treatment
  • 25% have cancer (permanent risk factor)
  • 25% have no identifiable risk factor
    • Need to consider undetected malignancy- evaluate risk factors e.g. smoking and cancer
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19
Q

Pancreatic cancer=

A

highest risk of DVT/PE

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20
Q

Hypercoagulable conditions

*

A
  • Hypercoagulation workup performed if no obvious cause for embolic disease- screen for:
    • Antithrombin III deficiency- natural blood thinner
    • Factor C or protein S deficiency or resistance
      • Factor V Leiden mutation- causing resistance to activated protein C is the most common risk factor for DVT/PE in younger people
    • Lupus anticoagulant
    • Homocystinuria
    • Occult neoplasm
    • Connective tissue disorders such as RA
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21
Q

sudden death in

A

20% - many asymptomatic

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22
Q

Pathophysiology of clinical outcomes in PE:

  • Acute right ventricular overload (death)
A
  1. Pulmonary artery pressure increases if more than 30% of the total cross section of pulmonary arterial bed occluded
  2. This leads to acute right ventricular dilatation and strain
  3. Also inotropes are released by the body in attempt to maintain systemic BOL these cause pulmonary artery vasoconstriction that further exacerbates situation- right heart collapse
  4. Main cause of death in PE is acute right sided heart failure leading to:
    1. Cardiogenic shock with circulatory failure
      • Increased afterload for RV Right heart collapse
      • Because the right ventricle is working so hard it pushes into the left ventricle through the interventricular septum
      • Decreases amount of space in LV
      • EDV decreased- preload decreases
      • Cardiogenic shock and death
    2. Cardiac arrest secondary to arrhythmias
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23
Q

Pathophysiology of clinical outcomes in PE:

  • respiratory failure
A
  1. Due to areas of ventilation perfusion mismatch
  2. Low right ventricle output
  3. Shunt with patent foramen ovale
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24
Q

Pathophysiology of clinical outcomes:

  • Pulmonary infarction
A
  1. Small distal emboli may create areas of alveolar haemorrhage
  2. Resulting in haemoptysis, pleuritis and small pleural effusion
    1. Pulmonary infarction
  3. Relatively uncommon- approx. 10-20% cases- may be visible on CXR as wedge shape
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25
Q
  • Symptoms of PE
A

some people have zero symptoms- need to consider PE in context of risk factors

  • dyspnea
  • pleuritic chest pain
  • cough
  • substernal chest pain
  • haemoptysis
  • syncope
  • unilateral leg pain
  • fever of less than 39oC
  • chest wall tenderness upon palpation without hisotry of trauma, may be sole physical finding in rare cases
26
Q
  • Haemoptysis-
A

coughing up blood

27
Q

signs of PE

A
  • tachypnea>16/min
  • rales or decreased breath sounds
  • accentuated second heart sounds
  • tachycardia
  • fever >37.8
  • diaphoresis
  • thrombophlebitis
  • lower extremity oedema
  • cardiac murmus
  • cyanosis
28
Q

diaphoresis

A

sweating

29
Q

Thrombophlebitis

A

(throm-boe-fluh-BY-tis) is an inflammatory process that causes a blood clot to form and block one or more veins, usually in your legs.

30
Q

IMPORTANT

A
  • Symptoms of PE may be mild and generally recognised symptoms may be absent in pts with the largest PE
  • High or intermediate probability objective clinical assessment may suggest need for diagnostic studies, but low probability objective clinical assessment may be present even in pts with PE
  • Maintenance of high level of suspicion is critical for the identification of pts in whom diagnostic tests may be necessary
    • History
    • Risk factors key
31
Q

Main differential diagnoses

A
  • Pneumothorax
  • Pneumonia
  • MI
  • Pericarditis
  • Pleurisy
  • Musculo-skeleta; chest pain
32
Q

Investigations

A
  • blood gases
  • CXR
  • ECG
33
Q
  • Blood gases
A
  • May show hypoxaemia and hypocapnia (resp alkalosis) due to hyperventilation
  • Undertake if evidence of hypoxaemia requiring oxygen
  • In a small proportion of pts arterial PaO2 may be normal
34
Q

CXR

A
  • By far most common finding in PE is a normal CXR
  • May be used to exclude other diagnosis
  • Not useful as primary diagnostic tool
  • Classic finding- peripheral wedge shape
35
Q

classic ECG finding in pulmoanry embolism

A

SIQIIITIII

36
Q

SI

A

deep S wave in lead I

37
Q

QIII

A

Q wave in III

38
Q

TIII

A

inverted T wave in III

39
Q

ECG will show

A
  • Signs of right ventricular strain
    • T wave inversion in V1-V4 and inferior leads II, III and aVF
  • Classic finding is SIQIIITIII
    • Deep s wave in lead I, Q wave in III, intervted T In III- 20% of pts with PE
      *
40
Q
  • People who have PE are prone to
A

Supraventiruclar Tachyarrhythmias

41
Q

further investigations

A

D -dimer

42
Q

what is D-dimer

A
  • Fibrin degradation product, a small protein fragment released into blood when a thrombus is degraded by fibrinolysis
43
Q
  • Normal D-dimer
A

rules out PE in those at LOW risk of PE

44
Q

in those at HIGH risk of PE, negative D-dimer

A
  • does not have a high enough negative predictive value need further imaging tests
45
Q

what is used to decide likelihood of PE

A

modified wells score

46
Q
  • Modified Wells score
    *
A
  • Stratify people into different risk categories, so that most appropriate diagnostic pathway or treatment pathways can be followed
  • Two risk categories
    • Likely
    • Unlikely
47
Q

Imaging for PE

A

CT pulmonary angiography (CTPA)

e.g. saddle embolus

48
Q

Treatment of PE

A
  • Do not forget oxygen
    • Decrease hypoxic vasoconstriction
  • Immediate heparinisation
    • Reduces mortality
    • Subcutaneous low molecular weight heparin used
49
Q

How does heparinisation reduce mortality

A
  1. Stops thrombus propagation in pulmonary arteries and allows body’s fibrinolytic system to lyse thrombus
  2. Stops thrombus propagation at the embolic source and reduces frequency of further pulmonary embolism
  3. Does NOT DISSOLVE THE CLOT- body does that
50
Q

what do we have to be careful with heparinisation

A

for heparin induced thrombocytopenia (0.1-0.2% )

51
Q

heparin induced thrombocytopenia (0.1-0.2% )

A
  • Heparin induced thrombocytopenia (HIT) most important and frequent drug induced, immune mediated type of thrombocytopenia
  • Much lower incidence with LMW heparin- but may still occur
  • Body produces antibodies to a portion of heparin that also recognise heparin-platelet complexes- binding of antibody to platelets activates them, platelet clumps are formed leading to thrombi
  • LOW PLATELET COUNT- but paradoxically increased risk thrombosis
  • Thromboembolic complications can be venous, arterial or both
    • Include DVT, PE, myocardial infarction, thrombotic stroke and occlusion of limb arteries
52
Q

treatment of heparin induced thrombocytopenia

A
  • immediate cessation of all formulations of heparin
    • But may not stop continuing thrombin generation nor avoid thrombotic events (40% pts)- need to use non-heparin based anti-coagulants
53
Q

Treatment of high risk PE patients

A
  • Haemodynamic support
  • Resp support
  • Exogenous fibrinolytics (streptokinase/tPA)
    • Peripheral intravenous
    • Delivered directly via a percutaneous catheter into the pulmonary arteries
  • Percutaneous catheter directed thrombectomy
  • Surgical pulmonary embolectomy
54
Q
  • Surgical pulmonary embolectomy
A
55
Q

What happens after initial heparinisation? Long term treatment

*

A
  • Oral anticoagulant e.g. warfarin or direct oral anticoagulant DOAC e.g. rivaroxaban now increasingly prescribed- lowerk risk bleeding
    • For 3 months if there is an identifiable temporary risk factor (50%)
    • Indefinitely if cancer or no identifiable risk factor (50%)
56
Q
A
57
Q
  • Which pts cannot be safely anticoagulated?
A
  • Oesophageal varices
  • Previous haemorrhagic stroke
  • Retroperitoneal bleed
  • Severe thrombocytopenia
58
Q

What if cant use any form of anti-coagulation

A

Inferior vena cava filter

59
Q

Prevention DVT/PE (outpatient)

*

A
  • Should an obese women who smokes me on COCPs or HRT
  • Advice for people with thrombophilia who travel >4 hours
60
Q
  • Prevention DVT/PE (Inpatient)
A
  • DVT prophylaxis after surgery
  • DVT prophylaxis for patients with malignancy
  • Reduce immobility
61
Q

Need to balance risk of DVT vs risks of

A

bleeding re active prophylaxis

Respiratory (27 decks)

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