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RESPIRATORY > Pulmonary Embolism and Pulmonary Hypertension > Flashcards

Pulmonary Embolism and Pulmonary Hypertension Flashcards

1
Q

What is meant by a pulmonary embolism?

A

blockage of a pulmonary artery by:

  • a blood clot
  • fat
  • tumour
  • air
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2
Q

What is meant by a pulmonary infarction?

A

Blood flow and oxygen to the lung tissues is compromised

=> Lung tissue may die

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3
Q

How are DVTs classified?

A

Proximal (Ileo-femoral)

Distal (Polpiteal)

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4
Q

Which type of DVT is most likely to embolise?

A

Proximal (ileo-femoral)

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5
Q

Distal DVTs are most likely to lead to chronic venous insufficiency and venous leg ulcers. TRUE/FALSE?

A

FALSE!

- Its actually proximal leg ulcers which cause these

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6
Q

How do DVTs usually present?

A
  • Whole leg or calf involved (depending on site)
  • Swollen
  • hot
  • red
  • tender
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7
Q

What are the potential differential diagnoses for a DVT?

A

Differential:

  • Popliteal synovial rupture (Baker’s cyst)
  • Superficial thrombophlebitis
  • Calf cellulitis
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8
Q

What Investigation is first line for DVT?

A

Ultrasound Doppler leg scan

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9
Q

Other than a Doppler US, what scan can be completed if you suspect a DVT?

A

CT scan of:

  • Ileo-femoral veins
  • IVC
  • pelvis
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10
Q

The DVT which predisposes a patient to a PE may be “silent” i.e. asymptomatic. TRUE/FALSE?

A

TRUE

=> first symptom they get may be that of a PE

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11
Q

Clinical presentation of a PE depends on its size. Describe the difference in presentation of varying sizes of PE.

A

Large:

  • shock (low BP)
  • central cyanosis
  • sudden death

Medium

  • pleuritic pain
  • haemoptysis
  • breathless

Small recurrent PEs

  • progressive dyspnoea
  • pulmonary hypertension
  • right heart failure
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12
Q

There are many Risk Factors for developing a DVT or PE. Name some of these

A

These usually come under Virchow’s Triad:

  • Stasis
  • Hypercoagulable state
  • Turbulent Blood flow/ Endothelial damage
Thrombophilia (hypercoag.)			
Contraceptive pill/HRT		
Pregnancy								
Pelvic obstruction
Trauma 
Surgery
Immobility e.g. bed rest, long haul flights
Malignancy		
Obesity
Pulmonary hypertension
Vasculitis
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13
Q

How are DVTs prevented in those who are at risk?

A
  • Early post-op mobilisation (prevent immobility)
  • TED compression stockings
  • Calf muscle exercises
  • LMWH perioperatively (Fragmin)
  • DOAC medications
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14
Q

Describe the findings on Arterial Blood Gases of a patients suffering from a PE?

A 
ABGs:
LOW PaO2 
LOW SaO2 
=> (Type 1 resp failure)
[PaCO2 can be normal or low]
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15
Q

Describe how a CXR of a PE can appear?

A
  • Normal early on before infarction
  • Basal atelectasis (collapse)
  • consolidation
    = Pleural effusion
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16
Q

What scoring systems can be used to predict if a patient has had a PE?

A

Wells Score (>4 = PE likely, >6 = HIGH RISK)

Revised Geneva Score (>10 = HIGH RISK)

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17
Q

How can you investigate a patient with a suspected PE?

A
  • Assess risk using the Pulmonary Embolism Severity Index (PESI)
  • ECG
  • D-dimers usually raised
  • Troponin +/- BNP
  • Isotope V/Q Scan
  • CT Pulmonary Angiogram (CTPA)
  • Leg/pelvic US for DVT check
  • ECHO
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18
Q

What are the advantages of a V/Q scan?

A
  • Sensitive for small peripheral emboli
  • Perfusion defect shows BEFORE infarction
  • Perfusion+Ventilation matched defect after infarction
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19
Q

What is the stereotypical ECG pattern of a patient with a PE?

A

Acute Right heart strain pattern => S1Q3T3

  • Prominent S wave in lead I
  • Q wave and inverted T wave in lead III
  • sinus tachycardia
  • T wave inversion in leads V1 - V3
  • Right Bundle Branch Block
  • low amplitude deflections
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20
Q

Why would you consider doing a CTPA in the context of a PE?

A
  • to image pulmonary artery filling defect

- to pick up larger clots in proximal vessels

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21
Q

Why would an ECHO be completed when investigating a PE?

A
  • measure pulmonary artery pressure
  • measure RV size
  • If RV is acutely dilated this is in keeping with acute PE
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22
Q

What underlying cause for a PE should be considered if there are no obvious causes? How would you investigate for these?

A
  • Consider cancer
    Check: CXR, PSA, CA125, Pelvic US or CT Abdo/pelvis
  • Autoantibodies (e.g. Antiphospholipid syndrome)
    Check: Anti-nuclear, Anti-Cardiolipin
  • Thrombophilia screen
    Check: Anti-thrombin-III deficiency, Protein C or S deficiency, Factor V Leiden
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23
Q

What investigation modality should be used for a suspected PE in a VERY unwell patient?

A

CTPA

24
Q

If a patient is admitted with a suspected low risk PE, and no previous respiratory disease (CXR NORMAL) what investigation should be done first?

A

Either - V/Q or CTPA

25
Q

If a patient with a suspected PE is pregnant, what investigation should be done first?

A

1st - US of legs

OR perfusion only scan (Q scan)
=> Avoid radiation to breast tissue where possible.

If VERY unwell = CTPA (accept risk of radiation)

26
Q

Where should patients with a PE be managed based upon their risk?

A 
Low risk = ambulatory care pathway -> home
Mid Risk = ward/ HDU if req'd
High risk (inc. cardiovascular compromise) = HDU (They may require thrombolysis)
27
Q

How is a DVT or PE usually treated?

A

Therapeutic dose of S/C LMWH
=> Dalteparin/Fragmin

  • give tx empirically if pt is high risk and you are awaiting test results
  • withhold tx for low risk pts until test results come back
28
Q

How is LMWH given and how long do patients continue on this for?

A
  • LMWH –once daily injection
  • no monitoring required
  • Start warfarin simultaneously
  • After 3-5 days stop heparin when INR>2
29
Q

What other type of drug can be used instead of LMWH and warfarin?

A

DOACs
Direct Factor Xa inhibitors
- Rivaroxaban
- Apixaban

30
Q

What are the INR targets for patients who have remained on warfarin?

A
  1. 0-3.0 (2.5) After 1st event
  2. 0 or more for recurrent events
  3. 5 if recurrent DVT/PE whilst on warfarin
31
Q

Warfarin interacts with many other substances. TRUE/FALSE?

A

TRUE

  • alcohol, antibiotics, grapefruit
  • Anti-platelets/ drugs which increase bleeding tendency
    e. g. Aspirin, NSAIDs, Clopidogrel

=> CHECK BNF

32
Q

When would thrombolysis be used to treat a PE?

A
  • life-threatening massive /sub-massive PE
  • low BP (sustained sys <90 mmHg for 15mins)
  • severe hypoxaemia
  • imminent or actual cardiorespiratory arrest
33
Q

What drug is used in thrombolysis?

A

tissue plasminogen activator (tPA) - tenecteplase

34
Q

Give some examples of the relative and ABSOLUTE contraindications to thrombolysis.

A

Relative:

  • Pregnancy/post partum
  • anticoagulants
  • TIA <6 months ago
  • advanced liver disease
  • active peptic ulcer disease

Absolute:

  • haemorrhagic stroke
  • ischaemic stroke <6 months
  • cerebral neoplasm or trauma
  • recent major trauma/surgery
  • known bleeding disorder
  • aortic dissection
35
Q

How long should treatment be continued for after having a PE?

A

Unprovoked 1st PE 6 months
Provoked PE / temporary risk factor 3 months
Unprovoked low-risk distal DVT 3 months
High risk proximal DVT 6 months
Recurrent DVT/PE Life-long

36
Q

IVDUs and patients with active cancer should be put on which type of anticoagulant?

A

LMWH (Fragmin)

- SHOULD NOT be given warfarin

37
Q

If a young male has a life threatening PE at first presentation and has a high risk of recurrence, how long should he continue his treatment for?

A
  • consider life long treatment after 1st event
38
Q

Patients on anticoagulation have a risk of bleeding/ being over-anticoagulated. How is this treated?

A
  • If bleeding STOP anticoagulant
  • reverse effect with antidote
  • LMWH and warfarin have long T1/2 => takes a while to leave system
  • Consider prothrombin complex concentrate or fresh frozen plasma
  • Reverse warfarin with vitamin K (esp. if liver disease)
  • Reverse LMWH with protamine
39
Q

The effect of DOACs cannot be reversed. TRUE/FALSE?

A

TRUE

- no antidote

40
Q

What is a normal pulmonary artery pressure and what does this rise to in Pulmonary Hypertension?

A

Normal mean pulmonary arterial pressure (mPAP)
= 12-20 mmHg

Pulmonary HT mPAP >25 mmHg

41
Q

How can the pulmonary artery pressure be measured?

A
  • Measured with right heart catheter (invasive)

- Systolic pulmonary arterial pressure can be estimated with ECHO doppler

42
Q

What are the two main types of Pulmonary Hypertension?

A

Pulmonary VENOUS HT

Pulmonary ARTERIAL HT

43
Q

Pulmonary VENOUS HT is caused by what?

A
  • left-sided heart disease

=> Left Ventricular Systolic Dysfunction

  • ischaemic
  • Mitral Regurgitation / Stenosis
  • Cardiomyopathy
44
Q

Pulmonary ARTERIAL HT is caused by what?

A
  • this is considered PRIMARY pulmonary HT
  • Hypoxic – COPD, Pulmonary fibrosis
  • Multiple PEs
  • Vasculitis
  • Drugs
  • HIV
  • Cardiac Left to right shunt – ASD, VSD
45
Q

What is cor pulmonale?

A
  • Right-sided heart disease
  • secondary to lung disease
  • Fluid retention due to hypoxia +/- right heart failure
  • Can complicate COPD, fibrotic lung disease, chronic PE etc
46
Q

What are the clinical signs of Pulmonary Hypertension and Right sided heart failure?

A
  • Central cyanosis
  • Dependent oedema (oedema in lower body due to gravity)
  • Raised JVP
  • Right ventricular heave at left parasternal edge
  • Murmur of tricuspid regurgitation
  • Enlarged liver (pulsatile)
47
Q

How can pulmonary hypertension be investigated?

A
  • ECG - Right bundle branch block
  • CXR – cardiomegaly
  • Sats and ABGs
  • Pulmonary function with DLCO (diffusion capacity)
  • ECHO
  • Right ventricular systolic pressure (RVSP)
  • Measure RV and LV dimensions and function
  • Measure mPAP
  • D dimers
  • VQ scan
  • CTPA
48
Q

How is Primary Pulmonary ARTERIAL HT treated?

A
  • prophylactic anticoag. (warfarin)
  • O2 if hypoxic
  • Pulmonary Vasodilators
    => Ca2+ channel blockers (oral nifedipine,diltiazem)
    => Endothelin antagonist (e.g. Bosentan)
    => PDE5-inhibitor (e.g. Oral Sildenafil)
    => Prostanoids (IV Epoprostenol or Inhaled Iloprost)
    => Soluble Guanylate Cyclase stimulator (Riociguat)

OR Lung Transplant

49
Q

What is Chronic Thromboembolic Pulmonary Hypertension (CTEPH)?

A

Pulmonary Hypertension caused by an accumulation of small PEs

50
Q

How is CTEPH treated?

A

Riociguat – pulmonary arterial vasodilator

Pulmonary endarterectomy (removing blood clots from lungs)
- curative (2% operative mortality)
51
Q

Describe how the pulmonary circulation supplies the lung

A

Dual supply
=> Pulmonary arteries
=> Bronchial arteries

52
Q

The Pulmonary artery receives the entire cardiac output TRUE/FALSE?

A

TRUE

53
Q

The pulmonary circulation is a low pressure system. What does this mean?

A
  • Thin walled vessels

- Low incidence of atherosclerosis

54
Q

Describe the pathological morphology of Pulmonary Hypertension

A
  • Medial hypertrophy of arteries
  • Intimal thickening (fibrosis)
  • Atheroma
  • RV hypertrophy
55
Q

What sign on CXR indicates Right sided heart failure?

A

Cardiomegaly

=> heart takes up more than 1/3 of CXR

RESPIRATORY (9 decks)

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