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- Y6 Respiratory > Pulmonary Embolism > Flashcards

Pulmonary Embolism Flashcards

1
Q

Define PE.

A

A consequence of thrombus formation within a deep vein of the body, embolising to pulmonary vasculature.

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2
Q

What is Virchow’s triad?

A
  1. stasis
  2. hypercoagulability
  3. vessel wall damage
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3
Q

Describe the epidemiology of PE.

A

Approximately 51% of DVTs will embolise to the pulmonary vasculature, resulting in a PE.

UK ~50,000 a year

1-1.5/1000 population per year

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4
Q

What are the risk factors for PE, relative to Virchow’s triad?

A

Vessel wall damage - cell damage –> thrombus formation at venous valves. Examples:

  • trauma,
  • previous DVT,
  • surgery,
  • venous harvest,
  • central venous catheterisation

Venous stasis - poor flow/stasis cause thrombi and result in valvular damage, further promoting thrombus formation. Stasis increased in:

  • >40yrs
  • immobility
  • general anaesthesia
  • paralysis
  • spinal cord injury
  • MI, stroke,
  • varicose veins,
  • advanced congestive HF,
  • advanced COPD

Hypercoagulability - inherited + acquired conditions:

  • cancer,
  • high oestrogen,
  • IBD,
  • nephrotic syndrome,
  • sepsis,
  • blood transfusion,
  • inherited thrombophilia
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5
Q

Name 5 types of inherited thrombophilia –> hypercoagulability.

A
  • Factor V Leiden mutation
  • Prothrombin gene mutation
  • Protein C and S deficiency
  • Antithormbin deficiency
  • Antiphospholipid antibody syndrome
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6
Q

Describe the consequences of pulmonary embolism on the heart.

A

Rarely de novo. Usually DVT –> emboli. Obstruction increases pulmonary vascular resistance (PVR) increasing the WORK or RIGHT ventricle –> increased HR (Frank-Starling). Eventually PVR is so high that there is

  • over-distension of the RV
  • increased RV end-diastolic pressure
  • decreased RV cardiac output —> decreased LV preload –> hypotension and shock
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7
Q

What are the differences between the thrombi formed in arteries and deep veins?

A

DVT = fibrin and entrapped erythrocytes (red clots). Platelet aggregation is not seen at the site of thombus attachment.

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8
Q

What percentage of pulmonary vasculature needs to be occluded to cause hypotension and shock?

A

In healthy individuals it can be as little as 50%

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9
Q

Symptoms of pulmonary embolism.

A
  • Feeling of apprehension
  • Cough (+haemoptysis)
  • Presyncope or syncope
  • Chest pain
  • Dyspnoea
  • Fever (in 10%)
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10
Q

What are the signs of pulmonary embolism on physical examination?

A
  • Hypotension (systolic BP<90mmHg)
  • Tachypnoea
  • Tachycardia
  • Elevated JVP (if cor pulmonale present)
  • Fever
  • HEAVES (sternal)
  • Accentuated pulmonary component of S2 (if cor pulmonale present)
  • Unilateral swelling/tenderness of calf
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11
Q

What initial and later investigations would you do for a PE?

A

History and examination, followed by 2 level Wells score to estimate clinical probability of PE.

Wells >4 then PE likely so:

  1. Admit
  2. Arrange immediate CTPA (or V/Q)
  3. Interim anticoagulation if delay

Wells 4 or less PE unlikely:

  • D-dimer test within 4 hours
  • Interim anticoagulation if delay
  • CTPA if positive D dimer -
  • Interim anticoagulation if delayed
  • Stop anticoagulation if negative CTPA

Other tests to consider:

  • Coagulation studies (INR, PT, aPTT to establish baseline)
  • ABG - hypoxia and hypocapnia
  • CXR
  • ECG
  • Lower limb USS
  • V/Q scan
  • Echo
  • U&E
  • Thrombophilia screen
  • BNP, NT-proBNP, H-FABP.
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12
Q

What are the Wells and Geneva scoring systems?

A
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13
Q

Describe the results of these scans in PE:

CTPA

V/Q scan

Bloods:

A

CTPA - direct visualisation of a thrombus in pulmonary artery (partial or incomplete)

V/Q scan - an area of ventilation will not be perfused in V/Q scan

Bloods:

  1. Coagulation studies - establish a baseline prior to commencing anticoagulation
  2. U&E - guide anticoagulation
  3. D-dimer - ELEVATED but should not be done if the likelihood of PE is already high
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14
Q

What might you see in CX of pulmonary embolism? What is sometimes seen on ECG?

A

CXR:

  • band atelectasis
  • elevation of hemidiaphragm
  • prominent central pulmonary artery (Fletcher’s sign)
  • oligaemia at site of embolism

ECG: “S1Q3T3” pattern of acute cor pulmonale is classic; this is termed the McGinn-White Sign. A large S wave in lead I, a Q wave in lead III and an inverted T wave in lead III together indicate acute right heart strain.

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15
Q

Why do you give IV fluids to someone with massive PE?

A

Given if systolic BP is <90mmHg

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16
Q

How do you manage a PE?

A

Emergency:

  • ABCDE
  • Respiratory support e.g. O2
  • Anticoagulation 3-6months e.g. rivaroxaban 15mg BD 3 weeks days followed by maintenance 20mg OD

Conservative:

  • Monitor anticoagulation
  • Provide leaflet on anticoagulation

Medical:

  • Anticoagulation 3-6 months
  • Thrombolysis - systemic or catheter-directed
  • Open pulmonary embolectomy

Surgical:

  • IVC filter -consider in those who cannot have anticoagulation
17
Q

Why do you give these treatments in massive PE w/ shock/hypotension?

Vasopressors

IV fluids

A

IV fluids - if systolic BP is <90mmHg but aggressive volume expansion is of no benefit and may worse RV function.

Vasoactive agents (noradrenaline/dobutamine/adrenaline) - if systolic BP is less than 90mmHg then these vasopressors may be given to improve RV function and RV coronary perfusion but should be limited to hypotensive patients.

18
Q

Which anticoagulants and thrombolytic therapy would you use in PE?

A

Offer:

1st line - apixaban or rivaroxaban

If these are not suitable: LMWH for at least 5 days followed by dabigatran or edoxaban.

Length of treatment depends on whether it is provoked or unprovoked.

19
Q

What are the complications of PE and its management?

A

Complications:

  • Acute bleeding during treatment
  • Pulmonary infarction
  • Cardiac arrest/death - due to acute RV failure
  • Chronic thromboembolic pulmonary hypertension
  • Heparin associated thrombocytopenia
  • Recurrent venous thromboembolic events
20
Q

What is the prognosis in PE?

A
  • If left untreated then prognosis is poor → chronic thromboembolic pulmonary hypertension → HF
  • Mortality rate is higher if patients are over 70, have cancer, CCF, COPD, systolic arterial hypotension, tachypnoea and RV hypokinesis on echo.
21
Q

How can you manage cardiac arrest due to PE?

A

Usual CPR, adrenaline +/- defibrillation if VF/VT

Can administer thrombolysis if patient is not responding to ALS

22
Q

What is the diagnosis?

A

Saddle PE - causing a PE on both the left and right sides.

- Y6 Respiratory (23 decks)

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