Venous thrombosis & Pulmonary embolism (PE) Flashcards
What is a DVT?
What is pulmonary embolism?
Deep vein thrombosis (DVT): thrombus formed in vein: almost always occurs in leg veins:
i) Distal – confined to calf veins
ii) Proximal – involve popliteal vein or above
Pulmonary embolism (PE): a dislodged thrombus (embolus) migrating to pulmonary vasculature
Where are DVTs most likely to occur? [1]
In the leg veins:
a) Distal veins - calves (e.g anterior / posterior tibial veins / )
b) Proximal veins - popliteal and above
(but can occur in upper body veins - e.g. axilla if long term IV canula in)
How do DVTs occur?
Muscle contraction AND vales causes venous return in legs.
If muscles dont contract: some valves dont open. Causes stagnant blood and clots to form above and below closed valves. **
When do eventually move muscles - clot leaves and becomes PE
How does PE occur?
Clot breaks off from PE
Normally small enough to pass through the right side of the heart
Enters into pulmonary circulation, where arteries narrow –> PE forms
What are 3 risk factors for thromboembolism - what is the name for these factors combined? [4]
Virchow’s Triad
Endothelial injury
Stasis or turbulence of blood flow
Blood hypercoagulability
Inflammation: causes procaogulant state - acts in combination with one of the above
Why might someone have hypercoaguable blood? [3]
When would you consider hypercoagulable states for DVT?
Why might someone have hypercoaguable blood?
- Antithrombin deficiency
- Protein C or S defiency (anti-coagulant proteins)
- Factor V Leiden mutation :causes resistance to activated protein C
Consider when no obvious signs for VTE/ PE
Name 4 risk factors for thromboembolism
Pregnancy: enlarged fetus compresses veins (increases venous stasis), increased production of clotting factors to stop bleeding during birth
Prolonged immobilisation
Previous VTE Event:: Previous valve damage; Underlying cause for previous VTE and not may be left untreated treated underlying cause then may cause again
Contraceptive pill & HRT
Long haul travel
Cancer: can damage endothelium wall; increased risk from clotting factors
Heart failure : poor circulation of vascular system; more likely to be immobile
Obesity
Surgery: causing endothelial damage; causing immoblisation; causes increase in clotting factors
Severge burns endothlial damage
Why does blood stasis increase risk of clot? [2]
What are 4 risk factors that cause reduced blood flow / blood stasis? [4]
Why does blood stasis increase risk of clot? [2]
- less release of NO and prostacyclin from endothelium when blood is static
What are 4 risk factors that cause reduced blood flow / blood stasis? [4]
Immobilisation in bed following surgery or other conditions eg hip/pelvis fracture
Long-haul flights especially >8hours (prolonged sitting )
Obesity causing reduced exercise and decrease in venous return in deep leg veins
Sickle cell disease: red cell precipitation can occlude vessels
Why does vein wall pathology increase chance of DVT / PE?
How can vein wall pathology / damage occur? [3]
Heparan sulfate projects out of the endothelial wall. These projections prevent platelet adhesion to intact endothelial membrane. If damaged - less heparan sulfate. increases risk of clot formation, especially if combined with reduced blood flow
Vein wall pathology can occur from:
a) smoking / alchohol
b) diabetes
c) chronic inflam disease (RA)
How do people present with DVT? [5]
Pain
Erythema (redness)
Tenderness
Swelling/oedema
Warmth
Superficial venous dilation
BUT: **often asymptomatic **
How do you diagnose DVT?
Use Wells’ Score:
- Add up points on the score: 2 points or more is likely. 1 is unlikely
- If 2 or more score: have proximal leg vein ultrasound
i) have positive scan - give treatment
iI) have negative scan, repeat in 6-8 days - do a D Dimer test
a) if D-dimer is positive: repeat scan in 6-8 days
b) if second sacan D-dimer is negative - consider alternative disease, but discuss symptoms with patient so they can look out for it - Venography - gold standard
* o D-dimer is fibrin degradation product
o Is a marker of fibrin formation
o Raised in VTE and other pathologies
D dimer: fibrin degradation product released when thrombus is degraded by by fibrinolysis low D dimer = low DVT risk.
Which 4 veins do DVT normally occur in? [4]
o Anterior tibial vein
o Popliteal vein
o Posterior tibial vein
o Peroneal vein
What are signs [4] and symptoms [4] of PE?
Signs:
- dyspnea
- pleuritic chest pain
- cough
- substernal chest pain
Symptoms:
- Tachypnea
- Decreased breath sounds
- Tachycardia
- Accentuated 2nd heart sound
- BUT: symptoms may be absent in patients with PE. SO need to consider history and risk factors*
How would you investigate for PE?
o Wells Score greater than 4
ECG - sinus tachycardia, right heart strain. T-wave inversion on anterior leads (V1-V3). Classic finding: S (deep S wave in lead I), Q ( present in lead III) and T (inverted T in lead III).
o CXR- possible small pleural effusion, peripheral wedge shaped density above diaphragm, focal oligemia. Most common finding with PE patients is a normal CXR, but used to excludes other diagnoses
o ABG - often hypoxic, low CO2 (due to hyperventilation)
Differential diagnose for EP
Pneumothorax – most closely follows symptoms of PE
Pneumonia
Myocardial infarction
Pericarditis
Pleurisy
Musculo-skeletal chest pain
Explain how PE can cause cardiac failure xx
- Right ventricle has thin muscle (pulmonary vasculature is a low pressure system)
- Increased pressure in the pulmonary vasculature due to PE
- Thin right ventricle has to work harder / dilates and is understrain
- Dilatation of right ventricle gets in the way of the left ventricle (pushes through interventricular septum) – less filling of the LV: fall in BP / decreased CO
- This causes release of adrenaline / noradrenaline: causes PE to vasoconstrict.
- Repeats cycle – can lead to MI / arrthymia
- So main cause of death is right sided heart failure leading to left sided heart failure cardiac arrest
- ALSO get patent foramen ovale in 1/3 patients: severe hypoxaemia & increased risk of stroke
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