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Respiratory > Pulmonary Embolism and Hypertension > Flashcards

Pulmonary Embolism and Hypertension Flashcards

1
Q

Describe a proximal (ilio-femoral) DVT.

A

Most likely to emobolise, most likely to lead to chronic venous insufficiency and venous leg ulcers.

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2
Q

Describe a distal (popliteal) DVT.

A

Least likely to embolise.

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3
Q

What is the clinical presentation of DVT?

A

Whole leg or calf involved depending on site. Swollen, hot, red, tender.

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4
Q

What is the differential diagnoses of DVT?

A

Popliteal synovial rupture (Baker’s cyst), superficial thrombophlebitis (inflammation of vein due to blood clot), calf cellulitis.

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5
Q

What investigations can you do for DVT?

A

Ultrasound leg scan (1st line): non-invasive, exclude popliteal cyst and pelvic mass.
CT scan: ileo-femoral veins, IVC and pelvis.

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6
Q

What is the clinical presentation of a large PE?

A

Cardiovascular shock, low BP, central cyanosis, sudden death.

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7
Q

What is the clinical presentation of a medium PE?

A

Pleuritic pain, haemoptysis, breathlessness.

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8
Q

What is the clinical presentation of a small recurrent PE?

A

Progressive dyspnoea, pulmonary hypertension and right heart failure.

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9
Q

Name of the risk factors of a pulmonary embolism.

A

Thrombophilia; contraceptive pill; HRT; pregnancy; pelvic obstruction e.g. uterus, ovary, lymph nodes; trauma e.g. road traffic accident; surgery e.g. pelvic, hip, knee; immobility e.g. bed rest, long haul flights; malignancy, obesity, pulmonary hypertension/vasculitis.

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10
Q

How can you prevent DVT/

A

Early post-op mobilisation;TED compression stockings; calf muscle exercises; subcutaneous low dose LMWH (low molecular weight heparin) perioperatively e.g. dalteparin and fragmin; direct oral anticoagulant (DOAC) mediation e.g. dabigatran (direct thrombin inhibitor), rivaroxaban/apixaban (direct inhibitor of activated factor Xa).

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11
Q

What will be the classic history of presenting complaint for PE?

A

SOB (often acute onset), chest pain (pleuritic), haemoptysis, leg pain/swelling, collapse/sudden death.

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12
Q

What are the clinical features of PE?

A

Tachycardia, tachypnoea, cyanosis, fever, low BP, crackles, rub, pleural effusion.

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13
Q

What will the arterial blood gases be like for a PE?

A

Low PO2 and SaO2, normal PaCO2 (type I respiratory failure).

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14
Q

What will show up on a CXR of PE?

A

Normal early on before infarction. May be basal atelectasis, consolidation, pleural effusion.

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15
Q

What is PESI?

A

Pulmonary embolism severity index.

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16
Q

What will show up in an ECG for a PE?

A

Acute right heart strain pattern (S1Q3T3, T inversion in V1-3).

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17
Q

Are D-dimers raised or lowered in PE?

A

Raised.

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18
Q

What other molecules can you test for in PE?

A

Troponin or BNP/pro-BNP.

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19
Q

What are the scans you can do for PE?

A

V/Q scan (sensitive for small peripheral emboli, perfusion defect before infarction, perfusion and ventilation matched defect after infarction), CT pulmonary angiogram (CTPA) (images pulmonary artery filling defect to pick up larger clots in proximal vessels), leg and pelvic ultrasound to detect silent DVT.

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20
Q

What would you measure in an echocardiogram in a PE?

A

Measure pulmonary artery pressure and right ventricular size; acute dilation of RV in keeping with PE. Left ventricle will be D shaped.

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21
Q

If there is no obvious underlying cause, what should you investigate?

A

Cancer, autoantibodies (SLE), thrombophilia screen (anti-thrombin-III deficiency, protein C or S deficiency, factor V Leiden, increased VIII).

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22
Q

What would the features of a low risk patient with PE be and what would be their treatment pathway?

A

Low PESI, -ve troponin, no oxygen, no co-morbidities. Ambulatory pathway -> home.

23
Q

What would the features of a high risk patient with PE be and what would be their treatment pathway?

A

Cardiovascular compromise, may require thrombolysis (BP monitoring, medical high dependency unit (MHDU)).

24
Q

Would you give IV heparin or SC LMWH to treat DVT/PE?

A

SC LMWH (rarely IV heparin).

25
Q

If someone is low suspicion of PE/DVT, should you treat them before results or not?

A

Await test results before treatment.

26
Q

What should the drug treatment for the first 2 days of a PE/DVT consist of?

A

Once daily injection of LMWH, start warfarin simultaneously.

27
Q

After 3-5 days, when should you stop giving heparin?

A

When INR>2.

28
Q

What other drugs could you use solely instead of LMWH and warfarin?

A

DOACs - dabigatran (thrombin inhibitor) or rivaroxaban/apixaban (factor X inhibitor). Are less hassle and in most cases as effective as heparin or warfarin.

29
Q

What should you monitor warfarin against?

A

INR.

30
Q

What are the target INR ranges of warfarin for 1st PE, recurrent events and then recurrent DVT/PE on warfarin?

A

2.0-3.0 1st event, 3.0 for more recurrent events, 3.5 if recurrent DVT/PE whilst on warfarin.

31
Q

What can warfarin potentially interact with?

A

Alcohol, antibiotics, amiodarine, cimetitine, grapefruit, anti-platelet drugs.

32
Q

What is the main drug used in thrombolysis?

A

Tissue plasminogen activator (tPA - tenecteplase).

33
Q

When would you use thrombolysis in PE?

A

For life threatening/sub-massive PE.

34
Q

When would you use an IVC filter?

A

Recurrent PEs.

35
Q

Other than thrombolysis and an IVC filter, what other treatments are there for PE?

A

Thromo-embolectomy (rarely indicated), intra-catheter thrombolysis, EKOS (ultrasound enhanced catheter thrombolysis).

36
Q

What are the estimated duration of treatment for unprovoked 1st PE, provoked PE/temp risk factor, unprovoked low-risk distal DVT, high risk proximal DVT, recurrent DVT/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 - lifelong.

37
Q

What drug would you give to an IV drug user or someone with active cancer with PE?

A

Fragmin only.

38
Q

Who else would you consider lifelong treatment for after 1st PE?

A

Life threatening PE at first presentation, especially young men who have a high risk of recurrence.

39
Q

What would you use to reverse the effects of warfarin and LMWH?

A

Vitamin K. Protamine.

40
Q

What mean pulmonary arterial pressure (mPAP) would be considered pulmonary hypertension?

A

> 25mmHg.

41
Q

What are the causes of pulmonary venous hypertension?

A

Left ventricular systolic dysfunction (ischaemic), mitral regurgitation/stenosis, cardiomyopathy e.g. alcohol, viral.

42
Q

What are the causes of pulmonary arterial hypertension (PAH)?

A

Primary pulmonary hypertension, hypoxia, multiple (chronic thromboembolic PH [CTEPH]) vasculitis (SLE, PAN, systemic sclerosis), drugs e.g. appetite suppressants, HIV, cardiac left to right shunt (septal defects).

43
Q

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

A

Central cyanosis if hypoxic, dependent oedema, raised JVP with V waves, right ventricular heave at parasternal edge, murmur of tricuspid regurg, enlarged liver (pulsatile).

44
Q

How would cor pulmonale show up on a CXR?

A

Cardiomegaly.

45
Q

What would you look for in an echocardiogram for cor pulmonale?

A

Right ventricular systolic pressure (RVSP), right ventricular dimensions and function, left ventricular dimensions and function, valvular disease.

46
Q

How do you measure mean pulmonary arterial pressure?

A

Cardiac catheterisation.

47
Q

What pharmacological treatment would you give for primary pulmonary arterial hypertension?

A

Prophylactic anticoagulation (warfarin), O2 if hypoxic, pulmonary vasodilators.

48
Q

What is the last line treatment for primary pulmonary hypertension?

A

Lung transplant.

49
Q

What is the drug used to treat chronic thromboembolic pulmonary hypertension?

A

Riociguat - pulmonary arterial vasodilator.

50
Q

What operation can be used to cure CTEPH?

A

Pulmonary endarterectomy.

51
Q

When would pulmonary infarction occur?

A

When there is a PE and bronchial artery supply is compromised.

52
Q

What are the mechanisms of pulmonary hypertension?

A

Hypoxia (causes vasoconstriction), increased flow through circulation (congenital heart disease), blockage (PE) or loss (emphysema) of pulmonary vascular bed, back pressure from left sided heart failure.

53
Q

Describe the morphology of pulmonary hypertension.

A

Medial hypertrophy of arteries, intimal thickening, atheroma, right ventricular hypertrophy, extreme cases (congenital heart disease, primary pulmonary hypertension).

54
Q

What are some of the signs of right heart failure?

A

Swollen legs, congested liver.

Respiratory (30 decks)

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