Pulmonary Embolism Flashcards
LOs
-Describe the types of pulmonary embolism -Basic science -Imaging -Treatments -Sequelae (condition that is the consequence of another) -controversies
Why do lungs get embolisms?
-All blood goes through the blood every 45 secs -Massive protective filter -Immune organ -Anti-inflam in highly oxidative environment -Capacity to cope- pneumonectomy survival
Types of embolism
Mycotic Fat Air Thrombotic
Mycotic embolus
transfer of infective pathogens to the lungs from a distant source
Fat embolus
-intravascular fat -often after fractures to the long bones- femur, tibia and pelvis -causes mulitfocal inflammatio in lungs
air embolism
air can escape from lungs into blood stream causes: -surface too quickly -iatrogenic: removing catheter, cannulation
Thrombotic embolism
coagulated blood -kirchows traid -usually from deep veins of the legs but consider other sites e.g. IV lines -paget schroetter syndrome (upper extremity DVT)
Clinical signs of PE
tachypnea rales (bubbling in the lungs tachycardia light headedness diaphoresis (excessive sweating) fever leg pain or oedema cyanosis clammy skin
janeway lesion
-small erythematous nodular lesions on the palms or soles -caused by infective endocarditis
osler node
red/purple raised bump with white centre found on fingers and toes -cause infective endocarditis
splinter haemorrhage
longitudinal- red brown haemorrhage under a nail -cause infective endocarditis
roth spot
a haemorrhage where ruptured blood vessels affect your retina seen on fundoscopy
kirchows triad
venous stasis endothelial disruption/ inflammation hypercoagulation / absence of clotting inhibition
Pulmonary embolism
-lung tissue is ventilated but not perfused as artery is occluded -intra-pulmonary deadspace –> impaired gas exchange -reduction in the cross sectional area of the pulmonary arterial bed -elevation in pulmonary arterial pressure -reduction in cardiac output -potential circulatory collapse and cardiac arrest due to RVF -alveolar collapse occurs, worsening hypoxaemia -unperfused lung may infarct but not likely due to bronchial circulation
outcomes of PE
-untreated PE mortality is high -67% of deaths are not diagnosed pre-mortem -treated PE mortality <5%
D-dimer
-breakdown product of fibrin in fribrinolysis of coagulated blood -indicates presence of large clot -95% sensitive (95% of time patients are correctly diagnosed) -50% (ability to correctly diagnose those without disease) -positive if above a threshold -over-measured due to fear of clinical criticism
Wells scoring system
A number that reflects your risk of developing DVT and is used in diagnosing PE. Pre-test tool used before D-dimer or CT-angiogram.
0-1: low risk
2-6: moderate risk
>6: high risk
Doppler ultrasound
Standard USS (ultrasound scan) technique- compressibility
Doppler allows assessment of the non-visualised venous system
- From CFV (common femoral vein) to diaphragm
- From PV (popliteal vein) to ankle
Excellent specifity and good sensitivity- operator dependant
V/Q test for diagnosing PE
A ventilation-perfusion scan
uses radioactive material to examine flow (ventilation) and blood flow perfusion) in the lungs
aim is to find the presence of any blood clots
Low dose and is useful in pregnancies
MRI scan for diagnosing PE
High specificity but low sensitivity
Expertise needed for interpretation
Long scan times, MRI unsuitable for acutely ill
Not really used
Echocardiography
Used to look at the heart and nearby vessels. A type of ultrasound.
Useful for assessing haemodynamic effects of current embolic burden
May suggest mortality -RV strain / coexistant heart disease
Poor sensitivity and specificity for PE
CTPA (CT- pulmonary angiography)
PIOPED II diagnostic criteria
83% sensitivity and 96% specific
Treatment for PE
Anticoagulants- initially LMWH then warfarin
Consider:
Rivaroxaban- compeitively inhibits free and clot bound factor Xa
Alteplase- thrombolytic, targets plasminogen and activates it
Warfarin
Dabigatran
Heparin
