Complex Critical Illness (ARDS) Flashcards
ARDS
complex syndrome characterized by:
1) non-cardiogenic pulmonary edema
2) severe hypoxemia (often resistant to O2 therapy)
3) characteristic CXR changes
4) decreased lung compliance
arises from direct insult (e.g. pneumonia) or indirect insults (e.g. pancreatitis, sepsis).
ARDS happens when…
out of control inflammatory response occurs in the lungs
a normal alveolar-capillary has…
a dry alveolus and perfused capillary
what are the three phases of ARDS?
exudative, proliferative, fibrotic
exudative phase
- begins 24hrs after insult
1) injury/insult to either capillary or alveolus
2) chemical mediators of inflmtn = injury to pulm capillaries = inc a/c membrane permeability = leakage of fluid filled with protein, blood, cells, fibrin to interstitial space + formation of microthrombi
3) pulm edema begins
- type 1 cells die
- compression of alveoli and small airways
clinical presentation in exudative phase
- restless, dyspnea, tachypnea
- coarse crackles
- mech vent needed
- CXR with patchy infiltrates
proliferative phase
- type 2 alveolar cells destroyed
- decreased surfactant production
- alveolar cells start to collapse
- oxygenation severely impaired
- CO2 removal continues
clinical presentation after proliferative phase
- SIRS fully manifested
- HI
- generalized edema
- worsening hypoxemia
fibrotic phase
- alveoli become enlarged and irregularly shaped (fibrotic)
- pulm capillaries become scarred
- continued stiffening of lungs inc pulm HTN
- continued hypoxemia
clinical presentation after fibrotic phase
MODS
refractory hypoxemia
increasing PaCO2
risk of pneumothorax
what would interstitial edema do to the O2 S+D?
thickened AC membrane
what would pulm edema do to the O2 S+D?
shunt/shunt like units
decreased SA
decreased compliance
what would alveolar compression/collapse do to the O2 S+D?
decreased SA
increased a/w
decreased FRC
decreased compliance
decreased volumes
increased demand (WOB)
what would loss of surfactant do to the O2 S+D?
decreased compliance
decreased volumes
increased demand
what would capillary damage and microemboli do to the O2 S+D?
dead space like
increased RV afterload
worsening PA pressures
what would progressive fibrosis and protein layer do to the O2 S+D?
thickened AC membrane
decreased compliance
decreased volumes
increased demand
ARDS pathology summary
- injury to lungs
- inflammatory process triggered
- chemical mediators released systemically and locally
- increased capillary permeability occurs
- fluid shifts across a-c membrane into interstitial space
- fluid and proteins into alveolar space = pulm edema
- V/Q mismatch of shunt and hypoxemia
- decreased diffusion, loss of SA, thickened AC membrane, and more hypoxemia
- decreased surfactant production and alveolar injury = decreased compliance and ventilation
ARDS resolution - fibroproliferative
- resolution of pulm edema
- protein based layer cleared
- type 2 cells multiply
- structural and vascular remodelling occurs
- damaged type 1 and 2 cells may be replaced by collagen/scar tissue
fibrotic alveoli affects the O2 supply and demand how?
decreased compliance
increased AC membrane thickness
fibrotic capillaries cause?
increased PVR/PAD
pulm HTN
ARDS Dx: Berlin Criteria
1) timing
2) chest imaging
3) origin of edema
4) oxygenation
berlin criteria: timing
within 1 week of known clinical insult or new/worsening resp symptoms (most ARDS pts identify within 72hrs)
berlin criteria: chest imaging
bilateral opacities, not fully explained by effusions, lobar/lung collapse, or nodules (white out, change may not be evident for 24hrs)
berlin criteria: origin of edema
resp failure not fully explained by cardiac failure or fluid overload. need to exclude hydrostatic edema if no risk factor present.
