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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?

Study These Flashcards
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?

Study These Flashcards
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?

Study These Flashcards
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
How is Warfarin treatment monitored?
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
What can warfarin interact with in the body?
* Alcohol * Antibiotics * Amiodarone * Cimetidine * Grapefruit * Anti-platelets or drugs that increase bleeding tendency (aspirin, NSAIDs, Clopidogrel)
27
What is the treatment of DVT/PE following initial treatment?
* 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
What is the long-term treatment for DVT/PE?
* Continue Warfarin for 3-6 months | * Monitor Warfarin with INR-Target range 2.5-3.5
29
What is the duration of treatment for DVT/PE?
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
How should treatment be altered for special groups of patients?
* 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
What are treatments for severe/life-threatening PE?
* 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
What is life-threatening PE?
Low BP (<90 mmHg for 15 mins) and severe hypoxaemia due to main pulmonary artery occlusion
33
What is the treatment for recurrent PEs?
* Life-long treatment or * IVC filter to prevent embolisation from large ileofemoral/IVC clot
34
What are the relative contraindications of PE treatment?
* Pregnancy/post partum * Anticoagulants * TIA <6 months * Refractory hypertension * Advanced liver disease * Active peptic ulcer disease * Refractory resuscitation
35
What are the absolute contraindications of PE treatment?
* 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
How is over-anticoagulation reversed?
* 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
What is pulmonary hypertension?
mPAP >25 mmHg | mean pulmonary artery pressure
38
What are the features of pulmonary circulation?
* Normally a high flow, low pressure system | * Normal mean pulmonary arterial pressure (mPAP) is 12-20 mmHg
39
How is pulmonary hypertension measured?
* 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
What are the causes of pulmonary venous hypertension?
* Left ventricular systolic dysfunction - ischaemic * Mitral Regurgitation/stenosis * Cardiomyopathy e.g. alcohol, viral
41
What is the difference between PVH and PAH?
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
What is the difference between primary and secondary pulmonary hypertension?
* Primary - no known cause | * Secondary - develops as a result of other diseases
43
What are examples of causes of secondary pulmonary hypertension?
* 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
What is Cor Pulmonale?
* Right heart disease secondary to lung disease e.g. COPD
45
What is the effect of Cor Pulmonale?
Fluid retention due to hypoxia +/- right heart failure
46
What are the clinical signs of pulmonary hypertension and right heart failure?
* 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
What are the investigations for pulmonary hypertension?
* 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
How is primary pulmonary hypertension diagnosed?
Diagnosis by exclusion of other secondary causes
49
What are signs of primary pulmonary hypertension?
Progressive SOBOE and signs of right heart failure
50
What is the prognosis of primary pulmonary hypertension?
Poor prognosis of 3 years without treatment
51
What are the pharmacologic treatments of primary pulmonary hypertension?
* 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
What are non-pharmacological treatments for primary pulmonary hypertension?
Lung transplant
53
What are the treatments for chronic thromboembolic pulmonary hypertension? (CTEPH)
* Riociguat – pulmonary arterial vasodilator * Pulmonary endarterectomy - curative (2% op. mortality) * Balloon angioplasty
54
What is CTEPH?
Complication of PE - persistent breathlessness even after PE is treated

Respiratory: Patient History, etc (10 decks)

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