Diagnosis and Treatment of Pulmonary Embolism Flashcards
(50 cards)
Why do emboli end up in the lungs?
All blood goes through the lungs
Lungs act as a protective filter - better able to deal with emboli than areas in systemic circulation such as the brain.
Why are the lungs an adapted organ to be the site of emboli/thrombi?
Immune organ - increased B and T cell response
Anti-inflammatory in highly oxidative environment
Have a high capacity to cope with some damage to lungs - shown by good survival after pneuomonectomy.
What are the different types of embolism?
Mycotic (infective)
Fat
Air
Thrombotic
Where to thrombotic pulomonary embolisms normally arise from?
Mostly from deep veins of the legs (iliac, femoral and popliteal)
Also be from IV lines or upper limb
What is Paget Schroetter related to upper limb thrombosis?
When the upper limb has an increased risk of a DVT in the axillary or subclavian veins due to extrinisic compression or repetitive injury
Often from the subclavian vein being pressed against the junction of the first rib and the clavicle
May be termed effort thrombosis.
What is a mycotic embolus?
A transfer of infective pathogens to lungs from a distant source
What are the common causes of a mycotic embolus?
Intravenous drug use - iatrogenic drug infusion, blood transfusions or illicit drug use.
Infective endocarditis.
What signs can indicate a mycotic emboli?
Oslers nodes, Janeway lesions, roth spots and splinter haemorrhages Indicates systemic emboli often from infective endocarditis.
Oslers nodes - digits, pink with pale centre, painful
Janeway lesions - non-painful, patches on palm of hands
Splinter haemorrhages - red/purple lines under nail bed following direction of nail growth.
Roth spots - small haemorrhages on eyes
How might infective endocarditis by indentified in the heart?
Ultrasound - greyscale (growth around the valve)
What imaging technique is commonly used to visualise a potential embolus/thrombus in the lungs?
Chest CT
Chest angiogram.
What causes a fat embolus?
Normally a fracture in a long bone - where large amounts of fat-containing bone marrow can be released.
Causes multifocal inflammation in the lungs.
What causes an air embolus?
Occurs from incorrect canulation that then allows gas into the veins
In most scenarios the lungs act as a filter and are able to deal with the air embolus
However, in certain scenarios such as (Osler-Weber-Rendu) can be fatal and care should be taken not to inject certain patients unnecessarily
What is Osler-Weber-Rendu syndrome?
How does this link to pulmonary embolus?
Is a genetic autosomal dominant condition
Causes the formation of AV anatamosis in the skin, mucosa, GIT and lungs etc.
These anastomosis already cause respiratory problems for the patient - hypoxemia, haemorrhage
Also allow passage of an emboli from pulmonary to systemic circulation (without return to the heart) this is known as a paradoxical emboli
May predispose the patient for a cerebral abscess or stroke.
How do patients with Osler-Weber-renu syndrome often present?
Most to least common symptoms
Nose bleeds
Skin, lips and mouth telangescesica
Pulomonary, hepatic AVMs
GIT bleeds
Cerebral AVMs
Spinal AVMs.
What is the consequence of a large air emboli in the heart?
Heart chamber does not fill with blood as is airlocked
Heart contracts around air
Causes sudden cardiocirculatory collapse and sudden death.
What is cardiocirculatory collapse?
Severe hypotension resulting in cerebral hypoperfusion and loss of consciousness
Decreased blood flow to organs can be fatal.
Cause of sudden death.
What is the dual circulation to the lungs?
How is this beneficial?
The pulomonary arteries supply deoxygenated blood to the lungs, which is them oxygenated and returned to the heart via the pulmonary veins
The bronchial arteries provide high pressure oxygenated blood to the lungs to supply the parenchyma, then drain back via the bronchial veins into systemic circulation.
Why are the lungs less sensitive to damage from emboli than other areas?
Dual circulation - pulmonary obstruction, bronchial arteries can oxygenate the tissue.
Abundant collateral circulation to different areas of the lungs.
Alveoli are full of air so simple diffusion will supply the cells to a degree.
Tissues are less sensitive to anoxia
Because of the extensive collateral circulation and the efficiency of gas transfer there is minimal impact on O2 saturation assuming the emboli are small and not continuously arriving.
How does the rate of thrombus/air emboli absorption vary from the lungs to other tissue?
The lungs absorbed all emboli faster than other tissue
However, thrombotic emboli always take longer to absorb than air in all tissue
The more sensitive to anoxia a tissue is the longer it will likely take to absorb an emboli.
What does Virchows triad state will increase the risk of thrombus formation?
Venous statis - immobile patients, long flight, after surgery etc
Endothelial disruption/surgery - around cannulas, central lines or from hypertension
Hypercoagulability - obesity, smoking, cancer, antiphospholipid syndrome.
How common is it for a DVT to form a PE?
50% untreated DVT will form a PE
What are some statistics showing why the number of pulmonary embolisms is so high?
80% of pelvic surgery patients develop DVT post surgery
- Common cause of adult sudden death, in patient death and all deaths.
The risk of DVT increases with age
What are the pathological consequences of a PE?
The lung tissue is ventilated but not perfused, this area of lung may infarct (chest pain) but often does not due to the collateral blood supply.
Results in intra-pulmonary dead space and impaired gas exchange (resulting in shortness of breath)
Reduction in cross-sectional area of the pulmonary arterial bed
Elevation of pulmonary arterial pressure
Reduction in cardiac output as left heart filling decreases, high RA pressure can reopen the patent foramen ovale.
Potential circulatory collapse and cardiac arrest due to RVD
Alveolar collapse occurs worsening hypoxemia.
What are the outcomes of a pulmonary embolism?
Untreated PE - 10% die within one hour and 30% die within 1 month
67% of deaths are not diagnosed pre-mortem
34% show rapid detrioration prior to death making them hard to treat fast enough
If PE is treated it reduces your risk of mortality by 5%
Recurrence depends on risk factors - 2 to 4% of people have reoccurences of which 5 to 7% are fatal.