Unit 9 Flashcards
pulm edema
pulm congestion in vessels, fluid accum in lungs/alveoli
what causes pulm edema
inc HCP
et pulm edema
usually LS CHF
non CV issues
which non CV issues may cause pulm edema
FVE
smoke inhalation
aspiratin
iv drug abuse
why FVE cause pulm edema
inc blood vol lt inc HCP
why may smoke inhalation from a fire cause pulm edema
inhalation of toxic fumes -> inflm -> altered perm -> fluid shift
why may iv drug use cause pulm edema
inc vessel perm, CNS depression -> issue with fluid exch
path of fluid movement in pulm edema
fluid moves from blood to IS spae to alveoli
what does accumulation of fluid in avleoli do to gas exchange
increases the distance req for GE + expands SA lt dec GE and dec lung fx
mnfts of pulm edema
productive frothy cough
dec lung compliance
wet crackles on ausc
why do pts w pulm edema have a prod frothy cough
mix of air and fluid causing frothy sputum
why do lungs have dec compliance in pulm edema
rt inc in fluid in lungs
tx for pulm edema
treat cause , resp support via O2 and ventilation
embolism
process of formation for an emboli
how does pulm embolism occur
clot in DV dislodges -> RA -> RV pulm circuit
where are thrombi in pulm ebolism usually located
arterial pulm v
what percent of pulm emboli are lethal
33%
where do majority of pulm emboli arise from
DVTs
which veins have inc incidence for emb fomration
iliac, popliteal, femoral
other causes of pulm emb
fat, air, amniotic fluid
how may fat cause a pulm emb
fat from bone marrow if bone is fractured, as bones are highly vascularized
how may amniotic fluid cause a pulm emb
if rupture of membs coincideds with rupture of vessels during birth. fluid contains some partiular matter
where do large pulm emboli usually lay
in the bifurcation of main pulm a.
what variable does pulm emboli change in the PV ration
P and V
if a pulm emboli begins as dvt, what happens next …
breaks off -> embolus -> thrombus in a. bed -> impaired perf
what do platlets do when they interact with an embolis
begin to degranulate
what happens when platelets degranulate in pulm embolism
rls of mediators
what does mediator rls in pulm emb cause
constr of brachial and pulm a
why is V affected in VP in pulm emb
bronchial constr
what does hemodynamic instability
blood vol, BP, blood flow
what type of broncho constr occurs in pulm emb
reflexive
what causes reflexive broncho constr
n. reflex by SNS
what is the benefit of reflexive broncho constr
no benefit
why does CO dec in pulm emb
dec blood flow to LS of heart dt obstr-> dec circulation
what happens to surfactant prod in pulm emb. why
dec bc adeq perf is needed for surfactant to form
what happens when there is dec surfactant
atelectasis
mechanism of dec surfactant prod
ischemia rt dec perf -> tissue damage -> dec surf
why does RS HF occur in pulm embol
RS is pumping against resistance -> hypertrophy of RV
what are mnfts of pulm emboli based on
location of embolis and size
mfnts of pulm embolism
chest pain
tachypnea
dyspnea
tachycardia
why may chest pain occur in pulm embolism
rt ischemia
why may tachypnea occur in pulm embolism
rt bronchospasm??
when does dyspnea occur in pulm embolism
if there is tissue damage
why does dyspea occur in pulm ebolism
dec sa for GE
why does tachycardia occur in pulm embolism
rt dec CO
is inc HR in pulm ebol compesnatory
YES
dx for pulm embolism
hx, px ABG LDH3 Lungscan CXR, CT angiogram
which dx test for pulm embolism is most affectve
angiogram, but it is also the most invasive
LDH3
lactase dehydrogenase
fx of LDH3
ez that is released when there is tissue damage in lung damage (serum marker) 3 is lung spec
what is the complete name for lung scan
lung scan 131 I-HSA, IV
“HSA” in lung scan 131 I-HSA
stands for human serum albumin
what is HSA labeled with when doing lung scan
With iodine 131, an isotope.
fx of a lung scan
to label :HSA and visualize its movement thru the pulm circulation.
how is a lung scan done
injected IV and then visualized. non invasive
Tx for pulm embol (stat)
size dependent
anticoagulants and thrombolytics
maintain CV fx
when do we use caution with anticoag and thrombolytics
in pts who are at risk for bleeding
why do we maintain CV fx when txing pulm embol
to avoid shock
pulm htn
htn within pulm circuit that is pathologic and is sustained a
what measurement indicates pulm htn
> 25mmHg
normal mmhg for pulm circuit
~15mmhg
what allows the pulm circuit to handle inc CO
low P, low resistance circuit, where blood is distributed over extensive vasculature
when is inc CO a problem for the pulm circuit
when there is resistance in the ciruit
3 cats of et for pulm htn
inc pulm vol (rt septum defect)
hypoxemia
inc pulm venous p
et for pulm htn: inc pulm vol
fetal septum between RA and LA doesnt fully close, so blood can move into RA from LA and go into pulm circuit again, inc Co
et for pulm htn: hypoxemia
hypoxic lung tissue vaso constricts to prevent mass rls of CO2 causing inc resistance
what does hypoxic peripheral tissue do
vasodilates vessels to remove excess CO2
what may cause inc in pulm venous P
LV dysfx -> LSHF
top 3 mnfts of pulm htm
dyspnea, syncope, chestpain on excertion
what other mfnts occur in pulm htn
those of RSHF rt RV pumping against resistance
fatigue
what do you see on a cxr of a pt with pulm htn
RS v hypertrophy prior to HF
tx of pulm htn
tx cause
dec progression
vasodilation w CA channel blocker
ARDS
str damage to cap wall and alveoli rt trauma of lung. gross, fatal, and rapid damage with acute onset
mortality in ards
40-60%
et of ards
aspiration (near drowning/GI content) drugs (recreational) inhaled gas or smoke infc (septic) trauma/shock (burns, fat embolism, chest trauma) inc blood transfusions
why is there and inc in perm in ards
rt pathologic accum of cells lt mediator rls
what mediators are rlsed inards
proteases, PAF
what type of exudate is rls in ards
protein rich
what does the protein rich exudate rlsed in ards cause
non permiable membraine forms on alveoli wall, no exch occurs
what does inc perm in ards allow
fluid, protein, cellular debris, platlets, blood cells to move out of vasculature and enter alveoli
what happens to neutrolphils in ards
rls free radicals, phospholipids, proteases
what happens when free radicals, phospholipids and proteases are rlsd in ards
endothelial and alveolar damage, imfl
how/why do proteins, cells and fluids enter alveoli in ards
inc permeability rt inflm creates larger cell junctions, allowing entrance of larger components
what type of edema occurs in ards
large vol with variety of components
what does large vol edema do in ards
dec compliance, vent, and GE
hyaline memb
imprevious layer that forms in ards blocking all GE
why is the term hyaline used in hyaline memb
because the memb has a shiny appearance
why does atelec occur in ards
def and inactivated surfactanct
what is detected in abg in ards
profound hypoxemia
when do mnfts for ards appear
within minutes
5 earliest mfnts of ards
dyspnea hypoxemia on abg tahcypnea resp alkilosis late metb acidosis
why does tachypnea occur in ards
compensatory response in attempt to deliver more air to lungs
why does resp alkilosis occur in ards
inc RR lt dec CO2. bicarbonate inbody picks up more H to make CO2, causing alkilosis
why does late metb acidosis occur in ards
inc lactic acid prod lt inc H+ in blood, rt anaerobic resp dt hypoxemia
6th mnft of ards
diffuse consolodation
tx of ards
complex early detection has better prognosis reverse cause resp support avoid complications
