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Respiratory Block > 4- clinical aspects of PE + pulmonary hypertension > Flashcards

4- clinical aspects of PE + pulmonary hypertension Flashcards

1
Q

what DVT are most likely and least likely to embolise?

A
  • proximal ones (ileo-femoral) are most likely to embolie and lead to chronic venous insufficiency + venous leg ulcers
  • distal (popliteal) are least likely to embolise
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2
Q

what is clinical presentation of DVT?

A
  • whole leg or calf
  • swollen, hot, red, tender
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3
Q

what are investigations you can do for DVT?

A
  • ultrasound doppler leg scan (1st line) = non-invasive, exclude popliteal cyst, pelvic mass
  • CT scan = iliofemoral veins, IVC and pelvis
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4
Q

why might DVT lead to PE with no-one noticing?

A

DVT can be silent (so can small PE)

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5
Q

what are risk factors for pulmonary embolism (other than virchow’s triad)?

A
  • thrombophilia = increased risk of blood clots -FH, frequency, site, age
  • contraceptive pill (particularly if smokes), 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 = inflammation of blood vessels
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5
Q

what are effects of
a) large PE
b) medium PE
c) small PE

A

a) cardiovascular shock, low BP, central cyanosis, sudden death
b)pleuritic pain, haemoptysis, breathless
c) progressive dyspnoea, pulmonary hypertension + right heart failure

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6
Q

what are non-drug preventions of DVT?

A
  • early post-op mobilisation
  • TED compression stockings
  • calf muscle exercises
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7
Q

what are drug treatments for DVT?

A
  • subcutaneously low dose low mol wt heparin perioperatively
  • direct oral anticoagulant (DOAC) medication = dabigatran - direct thrombin inhibitor or rivaroxaban/apixaban - direct inhibitor of activated factor Xa
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8
Q

what are common symptoms of DVT/PE?

A
  • shortness of breath (often acute onset)
  • chest pain (pleuritic)
  • haemoptysis
  • leg pain/swelling
  • collapse/sudden death
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9
Q

what are clinical features of PE?

A

tachycardia, tachypnoea, cyanosis, fever, low BP, crackles, rub, pleural effusion

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10
Q

what type of respiratory failure is commonly found in PE?

A

decreased PaO2 and SaO2 with normal PaCO2 so type 1 resp failure

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11
Q

what may be seen on chest xray for PE?

A
  • normal early on (before infarction)
  • basal (lower) atelectasis (collapse or incomplete inflation), consolidation (replacement of air with fluid, pus, blood or something else)
  • pleural effusion (fluid in pleural space)
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12
Q

what is the score used to estimate severity of PE?

A

pulmonary embolism severity index (PESI) = assessment of risk once diagnosis made

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13
Q

what is seen on ECG that suggests PE?

A

acute right heart strain

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14
Q

what is effect on D-dimers if PE?

A

D dimers raised = when negative can rule out PE

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15
Q

when would you do CT pulmonary angiogram in PE? what other tests can you do to check for clots ? hint: in leg

A

to pick up larger clots in proximal vessels

  • consider leg ultrasound to detect silent DVT
16
Q

when might you do an echocardiogram for PE?

A

measures same stuff as CT (RV size, pulmonary artery pressure, dilation etc) but can be used if too unwell to attend CT or in outpatient sitting

17
Q

why can V/Q scanning be good?

A

generally reserved as outpatient tool

role = other tests can pick up large clots in arteries, less sensitive in smaller peripheries so these allow to examine small perfusion in lung →if mismatch, suggests PE

18
Q

what is septal flattening?

A

RV squeezes LV so can’t fill (one reason that causes sudden death)

19
Q

what are the 4 main things to think about when considering underlying cause of PE?

A

surgery, pregnancy, malignancy, immobility

20
Q

what is mean points to remember about treatment for DVT and PE?

A
  • warfarin used to be used but now use DOAC’s e.g. rivaroxaban, apixaban
  • IV heparin very rarely used - can be used in acute care but uncommon

thrombolysis = tissue plasminogen activator (tPA) e.g. tenecteplase

→for life threatening massive/submassive PE

21
Q

how urgently do you need scan when you suspect PE?

A

as soon as possible, you can use judgment. sometimes you can just give pill and tell them to come in next day

22
Q

what non-drug treatment can be done for severe PE?

A

can also do intra-catheter directed thrombolysis for DVT or PE (can also use ultrasound enhanced catheter)

23
Q

how long should treatment be for:
- unprovoked 1st PE
- provoked PE/temporary 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 = life-long
24
Q

what are clinical signs of PE?

A
  • central cyanosis
  • leg swelling
  • raised JVP (sign of right heart strain)
  • RV heave at left parasternal edge
  • murmur of tricuspid regurgitation
  • load P2
  • enlarged pulsatile liver
25
Q

what is the normal mean arterial blood pressure in pulmonary circulation?

A

12-20 mmHg

26
Q

what is pulmonary hypertension defined as? (the number)

A

mean arterial blood pressure (mPAP) >25 mmHg

27
Q

how can systolic pulmonary arterial pressure be estimated?

A

non-invasively using echocardiography with Doppler ultrasound

28
Q

what are the causes of pulmonary hypertension (5 groups)?

A

group 1 = pulmonary arterial hypertension = narrowing + thickening of arteries →increased vascular resistance

group 2 = pulmonary venous hypertension = elevated pressure in pulmonary veins due to left heart dysfunction

group 3 = hypoxic pulmonary hypertension = chronic hypoxaemia in things like COPD and pulmonary fibrosis

group 4 = pulmonary embolism = chronic thromboembolic pulmonary hypertension (CTEPH), occurs from unresolved PE

group 5 = other rare or mixed diseases = conditions such as vasculitis (e.g., systemic lupus erythematosus, polyarteritis nodosa), certain drugs (e.g., fenfluramine), and HIV infection

29
Q

what investigations should be done if pulmonary hypertension?

A
  • D dimers and VQ scan if PE suspected
  • CT Pulmonary Angiogram
  • Cardiac MRI
  • Auto-antibodies if vasculitis suspected
30
Q

what is gold standard test for pulmonary hypertension?

A

echocardiogram - for measuring right ventricular systolic pressure (RVSP), right ventricular dimensions and function, left ventricular dimensions and function, and the presence of valvular disease

31
Q

what is primary arterial hypertension characterised by? can it be cured?

A
  • can’t be cured but can treat to alleviate symptoms, it’s rare and progressive common in young women
  • characterised by elevated blood pressure in pulmonary arteries →increased pulmonary resistance and heart strain
32
Q

what is clinical presentation of primary or idiopathic pulmonary arterial hypertension?

A
  • Progressive exertional breathlessness
  • Worsening pulmonary hypertension leads to right heart failure
  • Poor prognosis of 3 years without treatment
33
Q

what are treatment options for idiopathic or primary pulmonary arterial hypertension (PAH)?

A

= can’t be cured but can treat to alleviate symptoms

so prophylactic anticoagulation (warfarin) or pulmonary vasodilators (ONLY FOR PRIMARY DISEASE) e.g. Ca2+ channel blockers (diltiazem), endothelin antagonist (bosentan, macitentan), PDE5-inhibitor (Oral Sildenafil/Tadalafil), Prostanoids (IV Epoprostenol or Inhaled Iloprost), Soluble Guanylate Cyclase stimulator (Riociguat)

also lung transplant + oxygen

34
Q

what is CTEPH = chronic thromboembolic pulmonary hypertension?

A

= form of pulmonary hypertension caused by chronic obstruction of pulmonary arteries due to unresolved thromboembolic material

34
Q

what is treatment for CTEPH = chronic thromboembolic pulmonary hypertension?

A
  • Riociguat – pulmonary arterial vasodilator
  • Pulmonary endarterectomy = curative surgical procedure to remove thromboembolic material(2% operative mortality)

Respiratory Block (46 decks)

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