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Respiratory: Patient History, etc > Clinical Aspects of Pulmonary Embolism and Pulmonary Hypertension > Flashcards

Clinical Aspects of Pulmonary Embolism and Pulmonary Hypertension Flashcards

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1
Q

What are thromboembolic diseases?

A
  • Deep venous thrombosis (DVT)

* Pulmonary embolism (PE)

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2
Q

What is pulmonary embolism?

A

Blockage of a pulmonary artery by a blood clot, fat, tumour or air

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3
Q

What is pulmonary infarction?

A

If blood flow and oxygen to the lung tissues is compromised the lung tissue may die

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4
Q

What are 2 types of DVT?

A
  • Proximal (oleo-femoral) - most likely to embolise, most likely to lea to chronic venous insufficiency and venous leg ulcers
  • Distal (Polpiteal) - least likely to embolise
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5
Q

Why is Proximal (ileo-femoral) DVT high risk?

A
  • Most likely to embolise * Most likely to lead to chronic venous insufficiency and venous leg ulcers
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6
Q

What are clinical presentations of DVT?

A
  • Leg swollen, hot, red, tender

* Whole leg to calf involved depending on site

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7
Q

What are the differential diagnoses for DVT?

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

What is used to diagnose DVT?

A

Ultrasound - used to distinguish between differential diagnoses

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9
Q

What is used to investigate DVT?

A 
Ultrasound Doppler leg scan (1st line)			
* Non invasive			  
* Excludes popliteal cyst, pelvic mass
CT scan 
* Ileo-femoral veins, IVC and pelvis
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10
Q

What are the clinical presentations of PE?

A
  • Predisposing DVT may be silent

Clinical presentation depends on size

  • Large - cardiovascular shock, low BP, central cyanosis, sudden death
  • Medium - pleuritic pain, haemoptysis, breathlessness
  • Small recurrent - progressive dyspnoea, pulmonary hypertension, right heart failure
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11
Q

What are risk factors for DVT and PE?

A
  • Thrombophilia- FH, freq, site, age
  • Contraceptive pill (particularly if smokes), hormone replacement therapy
  • Pregnancy
  • Pelvic obstruction e.g. uterus, ovary, lymph nodes
  • Trauma
  • Surgery e.g. pelvic, hip, knee
  • Immobility e.g. bed rest, long haul flights
  • Malignancy
  • Pulmonary hypertension/vasculitis
  • Obesity - compression of veins, leading to PE
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12
Q

What can be done to prevent PE?

A
  • Early post-op mobolisation
  • TED compression stockings
  • Calf muscle exercises
  • Subcutaneous low dose low mol wt heparin (LMWH) perioperatively e.g. Dalteparin (Fragmin)
  • DOAC medication – direct oral anticoagulant

Novel Oral Anticoagulant (NOAC) medication

  • Diabigatran – direct thrombin inhibitor
  • Riveroxiban/Apixaban – direct inhibitor of factor Xa
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13
Q

What is the history of presenting complaint of a patent with PE?

A
  • Shortness of breath (often acute onset)
  • Chest pain (pleuritic)
  • Haemoptysis
  • Leg pain/swelling
  • Collapse / Sudden death
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14
Q

What are the clinical features of PE?

A

Tachycardia, tachypnoea, cyanosis, fever, Low BP, crackles, rub, pleural effusion

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15
Q

What tests are used to diagnose PE?

A
  • Arterial blood gases (ABGs) - decreased PaO2 and SaO2 (type 1 resp failure: PaCO2 normal or low)
  • CXR - Normal early on before infarction
    After infarction - basal atelectasis, consolidation, pleural effusion
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16
Q

What is a PESI score?

A

Pulmonary Embolism Severity Index - used to identify risk of PE, low PESI score = low risk

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17
Q

How is PE diagnosed?

A
  • ECG: Acute Right heart strain pattern (S1Q3T3; T inversion in V1-3)
  • D-dimers usually raised
  • Raised troponin levels - indicator of right heart strain
  • Isotope lung scan (Ventilation/Perfusion: V/Q)
  • sensitive for small peripheral emboli
  • Perfusion defect before infarction
  • Perfusion+Ventilation matched defect after infarction
  • CT pulmonary angiogram (CTPA) to image pulmonary artery filling defect - picks up larger clots in proximal vessels
  • Leg ultrasound to detect silent DVT
  • Echocardiogram to measure pulmonary artery pressure and right ventricular size (dilation of RV can indicate acute PE)
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18
Q

What are features of a PE on ECG?

A
  • Dilated right ventricle
  • Flattened septum
  • D-shaped LV - normally circular but flattened septum makes it appear d-shaped
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19
Q

What are investigations of underlying cause of PE?

A
  • Consider cancer – Clinical exam; CXR, PSA, CA125, CEA, Pelvic USS or CT Abdo/pelvis
  • Autoantibodies (SLE) – Antinuclear, Anti-Cardiolipin Abs
  • Thrombophilia screen
  • thrombophillic tendency: Anti-thrombin-III deficiency, Protein C or S deficiency, Factor V Leiden; increased VIII
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20
Q

When are investigations of underlying cause of PE considered?

A

Consider if no obvious underlying cause –e.g. surgery /pregnancy /malignancy /immobility

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21
Q

What factors indicate thrombophillic tendency on a thrombophilia screen?

A
  • Anti-thrombin-III deficiency
  • Protein C or S deficiency
  • Factor V Leiden
  • Increased VIII
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22
Q

Where are those at risk of PE best managed?

A
  • Low risk: low PESI, -ve troponin, no oxygen req, no co-morbitities = at home
  • High risk: cardiovascular compromise, may req thrmbolysis, BP monitoring = Medical High Dependency Unit (MHDU)
  • Intermediate risk/intermediate-high risk = ward or MHDU
23
Q

What is the treatment for DVT/PE?

A
  • Anticoagulation prevents clot propagation - does not directly dissolve clot, tips balance to thrombolysis so body dissolves clot
  • Therapeutic dose of s/c low mol wt heparin e.g Dalteparin (Fragmin)
  • Rarely IV heparin
  • Also start Warfarin at the same time as heparin
  • Oral thrombin inhibitor, Dabigatran or factor Xa inhibitor, Rivaroxaban can be used instead of Warfarin in combination with Heparin or as monotherapy
24
Q

When is treatment delivered in DVT/PE?

A
  • Empirical treatment if high clinical suspicion whilst await confirmation with investigations
  • If low suspicion, await test results before treatment
  • If moderate suspicion, weigh pros vs. cons of empirical treatment
25
Q

How is Warfarin treatment monitored?

A

With INR

  • 2.0 - 3.0 for 1st event
  • 3.0 or more for recurrent events
  • 3.5 if recurrent DVT/PE whilst on warfarin
26
Q

What can warfarin interact with in the body?

A
  • Alcohol
  • Antibiotics
  • Amiodarone
  • Cimetidine
  • Grapefruit
  • Anti-platelets or drugs that increase bleeding tendency (aspirin, NSAIDs, Clopidogrel)
27
Q

What is the treatment of DVT/PE following initial treatment?

A
  • Oral warfarin-takes 3 days - antagonises Vit K dependent prothrombin
  • After 3-5 days stop heparin - when INR>2
  • Or use NOACs without LMWH
28
Q

What is the long-term treatment for DVT/PE?

A
  • Continue Warfarin for 3-6 months

* Monitor Warfarin with INR-Target range 2.5-3.5

29
Q

What is the duration of treatment for DVT/PE?

A

Depends on balance of risk (recurrent clot vs bleeding)

  • 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
30
Q

How should treatment be altered for special groups of patients?

A
  • Intravenous drug abusers or patients with active cancer - Fragmin only, no Warfarin
  • For life threatening pulmonary embolism at 1st presentation, particularly in young men who have a high risk of recurrence (up to 30% at 5 years regardless of initial treatment) - consider life long treatment after 1st event
31
Q

What are treatments for severe/life-threatening PE?

A
  • Thrombolysis - tissue plasminogen activator (tPA) e.g. Tenecteplase
  • Thrombo-embolectomy
  • Intra-catheter directed thrombosis - can directly apply anti-coagulant/clot busters to clot itself rather than causing systemic thrombolysis
  • EKOS (ultrasound enhanced catheter thrombolysis)
32
Q

What is life-threatening PE?

A

Low BP (<90 mmHg for 15 mins) and severe hypoxaemia due to main pulmonary artery occlusion

33
Q

What is the treatment for recurrent PEs?

A
  • Life-long treatment
    or
  • IVC filter to prevent embolisation from large ileofemoral/IVC clot
34
Q

What are the relative contraindications of PE treatment?

A
  • Pregnancy/post partum
  • Anticoagulants
  • TIA <6 months
  • Refractory hypertension
  • Advanced liver disease
  • Active peptic ulcer disease
  • Refractory resuscitation
35
Q

What are the absolute contraindications of PE treatment?

A
  • Haemorrhagic stroke
  • Stroke of unknown origin
  • Ischaemic stroke <6 months
  • Cerebral neoplasm or trauma
  • Recent major trauma/surgery/head injury (3 weeks)
  • GI bleeding <3 months
  • Known bleeding disorder (haemophilia)
  • Aortic dissection
  • Non-compressible puncture (cannot stop bleeding with pressure)
36
Q

How is over-anticoagulation reversed?

A
  • Address underlying cause - e.g. drug interaction, chronic liver disease, CHF
  • If bleeding then stop anticoagulant and reverse effect
  • Low MW Heparin has a long half life
  • Warfarin has a long half life
  • May need cover with prothrombin complex concentrate or fresh frozen plasma
  • Reverse warfarin with vitamin K1 (especially if chronic liver disease)
  • Reverse heparin with protamine
  • No reversal agent available for NOACs
37
Q

What is pulmonary hypertension?

A

mPAP >25 mmHg

mean pulmonary artery pressure

38
Q

What are the features of pulmonary circulation?

A
  • Normally a high flow, low pressure system

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

39
Q

How is pulmonary hypertension measured?

A
  • Measured with right heart catheter (invasive)
  • Systolic pulmonary arterial pressure can be estimated with ECHO doppler (possible pulmonary hypertension if >40mmHg in peripheral arteries)
40
Q

What are the causes of pulmonary venous hypertension?

A
  • Left ventricular systolic dysfunction - ischaemic
  • Mitral Regurgitation/stenosis
  • Cardiomyopathy e.g. alcohol, viral
41
Q

What is the difference between PVH and PAH?

A

Pulmonary venous hypertension (PVH) differs from PAH in that high blood pressure occurs when the heart can’t efficiently carry blood away from the lungs

42
Q

What is the difference between primary and secondary pulmonary hypertension?

A
  • Primary - no known cause

* Secondary - develops as a result of other diseases

43
Q

What are examples of causes of secondary pulmonary hypertension?

A
  • Hypoxic – COPD, OSA, Pulmonary fibrosis
  • Multiple PE – chronic thromboembolic PH (CTEPH)
  • Vasculitis –e.g. SLE, PAN, systemic Sclerosis
  • Drugs e.g. appetite suppressants - fenfluramine and derivatives
  • HIV
  • Cardiac Left to right shunt – ASD, VSD
  • Primary pulmonary hypertension
44
Q

What is Cor Pulmonale?

A
  • Right heart disease secondary to lung disease e.g. COPD
45
Q

What is the effect of Cor Pulmonale?

A

Fluid retention due to hypoxia +/- right heart failure

46
Q

What are the clinical signs of pulmonary hypertension and right heart failure?

A
  • Central cyanosis if hypoxic
  • Dependent oedema
  • Raised JVP with V waves (due to secondary tricuspid regurg)
  • Right ventricular heave at left parasternal edge
  • Murmur of tricuspid regurgitation
  • Load P2
  • Enlarged liver (pulsatile)
47
Q

What are the investigations for pulmonary hypertension?

A
  • ECG – rhythm, axis, p pulmonale, right bundle branch block
  • CXR - cardiomegaly
  • SaO2 and arterial blood gases
  • Pulmonary function incl DLCO (diffusion capacity)
  • Echocardiogram – estimate right ventricular systolic pressure (RVSP)
  • Cardiac Catheterisation – measure mean pulmonary arterial pressure (mPAP)
  • D dimers and VQ scan if PE suspected
  • CT Pulmonary Angiogram
  • Cardiac MRI
  • Auto-antibodies if vasculitis suspected
48
Q

How is primary pulmonary hypertension diagnosed?

A

Diagnosis by exclusion of other secondary causes

49
Q

What are signs of primary pulmonary hypertension?

A

Progressive SOBOE and signs of right heart failure

50
Q

What is the prognosis of primary pulmonary hypertension?

A

Poor prognosis of 3 years without treatment

51
Q

What are the pharmacologic treatments of primary pulmonary hypertension?

A
  • Prophylactic anticoagulation (warfarin)
  • O2 if hypoxic
    Pulmonary vasodilators
  • Ca2+ channel blockers (oral nifedipine ,diltiazem)
  • Endothelin antagonist (Oral Bosentan, Macitentan)
  • PDE5-inhibitor (Oral Sildenafil/Tadalafil)
  • Prostanoids (IV Epoprostenol or Inhaled Iloprost )
  • SolubleGuanylate Cyclase stimulator (oral Riociguat)
52
Q

What are non-pharmacological treatments for primary pulmonary hypertension?

A

Lung transplant

53
Q

What are the treatments for chronic thromboembolic pulmonary hypertension? (CTEPH)

A
  • Riociguat – pulmonary arterial vasodilator
  • Pulmonary endarterectomy - curative (2% op. mortality)
  • Balloon angioplasty
54
Q

What is CTEPH?

A

Complication of PE - persistent breathlessness even after PE is treated

Respiratory: Patient History, etc (10 decks)

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