4- clinical aspects of PE + pulmonary hypertension Flashcards
what DVT are most likely and least likely to embolise?
- 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
what is clinical presentation of DVT?
- whole leg or calf
- swollen, hot, red, tender
what are investigations you can do for DVT?
- ultrasound doppler leg scan (1st line) = non-invasive, exclude popliteal cyst, pelvic mass
- CT scan = iliofemoral veins, IVC and pelvis
why might DVT lead to PE with no-one noticing?
DVT can be silent (so can small PE)
what are risk factors for pulmonary embolism (other than virchow’s triad)?
- 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
what are effects of
a) large PE
b) medium PE
c) small PE
a) cardiovascular shock, low BP, central cyanosis, sudden death
b)pleuritic pain, haemoptysis, breathless
c) progressive dyspnoea, pulmonary hypertension + right heart failure
what are non-drug preventions of DVT?
- early post-op mobilisation
- TED compression stockings
- calf muscle exercises
what are drug treatments for DVT?
- 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
what are common symptoms of DVT/PE?
- shortness of breath (often acute onset)
- chest pain (pleuritic)
- haemoptysis
- leg pain/swelling
- collapse/sudden death
what are clinical features of PE?
tachycardia, tachypnoea, cyanosis, fever, low BP, crackles, rub, pleural effusion
what type of respiratory failure is commonly found in PE?
decreased PaO2 and SaO2 with normal PaCO2 so type 1 resp failure
what may be seen on chest xray for PE?
- 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)
what is the score used to estimate severity of PE?
pulmonary embolism severity index (PESI) = assessment of risk once diagnosis made
what is seen on ECG that suggests PE?
acute right heart strain
what is effect on D-dimers if PE?
D dimers raised = when negative can rule out PE
when would you do CT pulmonary angiogram in PE? what other tests can you do to check for clots ? hint: in leg
to pick up larger clots in proximal vessels
- consider leg ultrasound to detect silent DVT
when might you do an echocardiogram for PE?
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
why can V/Q scanning be good?
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
what is septal flattening?
RV squeezes LV so can’t fill (one reason that causes sudden death)
what are the 4 main things to think about when considering underlying cause of PE?
surgery, pregnancy, malignancy, immobility
what is mean points to remember about treatment for DVT and PE?
- 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
how urgently do you need scan when you suspect PE?
as soon as possible, you can use judgment. sometimes you can just give pill and tell them to come in next day
what non-drug treatment can be done for severe PE?
can also do intra-catheter directed thrombolysis for DVT or PE (can also use ultrasound enhanced catheter)
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
- 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
what are clinical signs of PE?
- 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
what is the normal mean arterial blood pressure in pulmonary circulation?
12-20 mmHg
what is pulmonary hypertension defined as? (the number)
mean arterial blood pressure (mPAP) >25 mmHg
how can systolic pulmonary arterial pressure be estimated?
non-invasively using echocardiography with Doppler ultrasound
what are the causes of pulmonary hypertension (5 groups)?
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
what investigations should be done if pulmonary hypertension?
- D dimers and VQ scan if PE suspected
- CT Pulmonary Angiogram
- Cardiac MRI
- Auto-antibodies if vasculitis suspected
what is gold standard test for pulmonary hypertension?
echocardiogram - for measuring right ventricular systolic pressure (RVSP), right ventricular dimensions and function, left ventricular dimensions and function, and the presence of valvular disease
what is primary arterial hypertension characterised by? can it be cured?
- 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
what is clinical presentation of primary or idiopathic pulmonary arterial hypertension?
- Progressive exertional breathlessness
- Worsening pulmonary hypertension leads to right heart failure
- Poor prognosis of 3 years without treatment
what are treatment options for idiopathic or primary pulmonary arterial hypertension (PAH)?
= 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
what is CTEPH = chronic thromboembolic pulmonary hypertension?
= form of pulmonary hypertension caused by chronic obstruction of pulmonary arteries due to unresolved thromboembolic material
what is treatment for CTEPH = chronic thromboembolic pulmonary hypertension?
- Riociguat – pulmonary arterial vasodilator
- Pulmonary endarterectomy = curative surgical procedure to remove thromboembolic material(2% operative mortality)
