12/13 Pulm Vascular Disease/PE - Jagpal Flashcards
pulmonary circulation
resistance/pressure
diseases of pulm circulation
pulmonary circl has LOW RESISTANCE
pulm bp is approx 1/8th systemic bp
segment : disorders
- artery : multiple
- embolic (thrombi, fat, amniotic fluid)
- pulmonary arterial HTN
- reactive pulmo vasoconst
- vasc abnormalities
- idiopathic pulm HTN
- elevated venous pressure
- incr pulmo blood flow
- capillary : capillaritis
- vein : pulm veno-occlusive disease (occult, hard to find/dx)
fat embolus
pathology
setting
key facts
path: occlusion of pulmo arteries by fat globules
setting: closed fractures of long bones or pelvis which releases fat from bone marrow
keys:
- latency period followed by ARDS (acute hypoxia, bilateral 4quad infiltrates, Pa/Fi (O2) ratio, exclusion of cardiogenic pulm edema)
- supportive tx indicated
amniotic fluid embolus
pathology
setting
key facts
path: occlusion of pulm arteries by lipoproteins
setting: delivery, premature rupture of amniotic sac
keys:
- amniotic fluid enters mom’s blood through placenta → allergic rxn to fluid leading to cardiopulm collapse
- tx is supportive
pulmonary embolus
basics
risk factors
how do emboli cause atelectasis?
blood clots that occlude pulmo arteries
- 95% of thrombi arise in deep venous system of lower extremities
- response depends on size and number of emboli, status of CV system
three key risk factors (Virchow’s triad):
- hypercoaculability
- vascular stasis
- endothelial damage
emboli → atelectasis. how?
- type 2 pneumocytes make surfactant which prevents atelectasis
- emboli disrupt perfusion → type 2 pneumos die → surfactant decreases → atelectasis ensues
major pathophysiological changes in acute PE
4x abnormality → clinical correlate
- mechanism
- hypoxemia → cyanosis
* V/Q mismatch: - atelectasis → dyspnea/rales on exam
* decr surfactant - incr pulmonary artery pressure →incr P2 on auscultation
* obstruction of pulmo arteries: need to try to reverse ASAP!!! - incr alveolar ventilation → tachypnea
* incr dead space ventilation, so incr RR to compensate
embolism without infarct
vs
embolism with infarct
without infarct
- multiple small emboli to lungs
- sudden onset dyspnea and tachypnea
- auscultation: few rales and decr breath sounds
with infarct - more pain, more breathless
- occluding thrombus and infarction
- auscultation: few rales,, decr breath sounds, friction rub
clinical presentation: PE
classic sx: dyspnea, pleuritic chest pain, hemoptysis
- THESE ARE NOT ALWAYS PRESENT
- SIGNS/SX ARE OFTEN ATYPICAL
signs and sx can often be obscured by co-existing disease
acute PE signs and symptoms
- dyspnea, wheezing, crackles
- pleuritic chest pain
- cough, hemoptysis
- tachypnea (20+ RR), tachycardia (100+ HR)
- fever
- cyanosis
- loud P2
- leg swelling and pain
gas exchange abnormalities in acute PE
classic pattern:
- hypoxemia
- incr A-a gradient
- respiratory alkalosis
application: the pattern is NOT universal! can’t use it to rule PE in or out
massive PE
- acutely elevated PA pressure
- hemodynamic instability
- CXR: vascular markings
- high mortality rate
- requires intensive approach to tx
diagnosis of PE
- clinical and lab evaluation
- clinical suspicion: Virchow’s triad
- history/physical
- ABG looking for hypoxemia
- D dimer
- assess bleeding risk
- apply PE probability test (ex. Wells score)
* helps determine need for imaging (sometimes in combo with D dimer) - imaging/studies
- ECG
- diagnostic radiology (CT with contrast, V/Q scan, Doppler ultrasound of lower extremities, pulmo angiogram with contrast)
what will you see on EKG with pulmonary HTN???
RVH!
- right axis deviation (past 90deg)
- tall R waves in RV leads
- deep S waves in LV leads
- possibl incomplete RBBB
- signs of RA enlargement
pulmonary arterial HTN
requirements to rule in
classification
based on measurements from right heart catheterization at rest
- mean PA pressure > 25
and
- pulmo cap wedge pressure < 15
allows us to rule out L sided heart disease to rule in PA HTN
classification of pulmo HTN
- pulmonary arterial HTN
- mostly women, ages 20-40
- idiopathic or primary PH; some genetic susceptibility
- death within 2-5yr
- no prodrome; late sx: dyspnea, fatigue, chest pain
- PH with left heart disease
- most common cause: incr L heart resistance to blood flow
- use plum cap wedge pressure to see if L heart involved
- PH assoc with lung disease and/or hypoxemia
- parenchymal lung disease or sleep conds
- increase oxygen! maybe
- PH due to chronic thrombotic and/or embolic disease
- misc (HIV, hepatic disease, sarcoidosis, IV drug use)
