ARDS Flashcards
What is ARDS
systemic process - lung MODS
non-cardiogenic pulmonary edema
severe hypoxemia resistant to oxygen
decreased lung compliance
T or F ARDS can be caused directly or by indirect injury
true
what are 6 direct ways ARDS can be caused
aspiration near drowning toxic inhalation pulmonary contusion pneumonia oxygen toxicity
what are 6 indirect injury causes of ARDS
sepsis non-thoracic trauma hypertransfusion severe pancreatitis shock states drug overdose: ASA, opioids, cocaine
What is the major precipitating event for ARDS
Sepsis
What are the ABCCs of infection/inflammation
arachdonic
bradykinin
coagulation
complement
what is the end result of the arachadonic pathway in the ABCCs of infection/inflammation
vasodilation
vasoconstriction
increased permeability
what is the end result of the bradykinin pathway in the ABCCs of infection/inflammation
potent vasodilation
increased permeability
what is the end result of the coagulation pathyway of ABCCs of infection/inflammation
micro-emboli formation
what is the end result of the complement pathway of ABCCs of infection/inflammation
intensify inflammation
damage endothelium
cell adhesion and death
What 3 things that occur in sepsis can lead to the cause of ARDs
vasodilation
capillary permeability
maldistribution of blood flow
what do the ABCCs of infection/inflammation do to cause ARDs
alveolar epithelial changes
airway changes
endothelial changes
what are the 4 stages of ARDs
exudative
proliferative
fibrous
resolution
when does the exudative phase occur
w/in 24-72 hours
when does the proliferative stage occur
day 2-10
when does the fibrous stage occur
> 10 days
when does resolution occur
several weeks
What happens in the exudative phase (5)
inflammatory mediators increase permeability of capillary membrane
fluid rich with protein, blood cells and fibrin leaks into pulmonary interstitium
alveolar cells type 1 - wall integrity becomes compromised
alveolar cells type 2 - damage causes loss of surfactant
microemboli cause pulmonary artery pressure to rise
What occurs in the fibroproliferative phase (4)
disordered healing
cellular granulation and collagen deposition occur within the alveolar-capillary membrane
alveoli become enlarged and irregular shaped (fibrotic)
further stiffening and decreased compliance increasing pulmonary HTN and hypoxemia
What occurs in the resolution phase (2)
recovery occurs over several weeks
structural and vascular remodeling takes place to re-establish alveolar-capillary membrane
What imaging is done to support a diagnosis of ARDs what does it look like
bilateral opacities - not fully explained by effusions, lobar/lung collapse nodules
‘white out’
What do we look at to quantify intrapulmonary shunting
PaO2/FiO2 ratio
what is a normal PaO2/FiO2 ratio
> 300 mmHg
what is the numeric value for normal intrapulmonary shunt
3-5%
What defines mild ARDs
PaO2/FiO2 200-<300 w PEEP or CPAP > or = 5
What defines moderate ARDs
100 -200 < PaO2/FiO2 with peep >/= 5
Shunt 15-20%
what defines severe
= 100 PaO2/FiO2 with Peep >/= 5
> 20% shunt
what will initial ABGs show for ARDs
hypoxemia
respiratory alkalosis from breathing off CO2
increased RR
What happens to a patients RR as ARDS progresses
decreases d/t fatigue
If you have a PA line in an ARDs pt what will you see
increased PADP while PCWP is unaffected
increase in difference >1-4 mmHg
What type of history would lead us to suspect ARDs
direct pulmonary insult or systemic inflammation
what timing would lead us to suspect ARDs
within a week of worsening symptoms
what types of assessment findings would lead you to suspect ARDs
coarse crackles in lung fields
High PIP and/or plateau pressures indicating worsening compliance
what are two ventilator findings that would indicate ARDs
increased PIP and Plateau pressures indicating worsening compliance
What diagnostic findings would indicate ARDs (3)
patchy infiltrates or opacities on CXR
non-cardiac pulmonary edema
worsening PaO2/FiO2 ratio
What part of cardiac output does ARDs affect
increased rt ventricular afterload causes decreased CO
what type of V/Q mismatch occurs in ARDs
both!
Shunting - thickened A-C membrane and inc. airway resitance
deadspace - micro-emboli form pulmonary HTN
what are early systemic findings in ARDs by system
CNS - restlessness
CVS - tachycardia
GI/GU - no appetite decreased UO
what Lab values would you see in early ARDs
low pO2
low CO2
alkalotic pH
SvO2 low
What systemic findings would you see later in ARDs
CNS - agitation, fatigue
CVS - tachycardia, full blow s/s of decreased afterload generalized edema
multiorgan involvement
what lab values would you see later in ARDs
resp acidosis
inc lactate
low SvO2
OER inc
what is the 2 pronged approach to treatment of ARDs
- treat causative factor if able - i.e pneumonia abx
2. support physiological fn and cellular oxygenation until the effects of ARDs/SIRS subside
what are the 4 areas of treatment to support ARDS pts
MV
hemodynamic support
positioning
pharmacology
What are 3 MV protective lung strategies for pts with ARDs
maintain plateau pressures < 30 cm H20
use low tidal volumes
permissive hypercapnia
What does PIP reflect
lung compliance and airway resistnace
is PIP representitive of static or dynamic compliance
dynamic
what is normal PIP
< 40 cm H20
When is a plateau pressure measured
end of inspiration when the lung is fully inflated but no air is moving in or out
what is plateau pressure representive of
lung compliance
is plateau pressure dynamic or static
static
what value is most accurate in determining lung compliance
plateau pressure
what is normal PP
25-30 cm H2O
what button is pressed to determine PP
end-inspiratory hold button
What ventilator settings have a decreased mortality and ventilator days in ARDS
TV <6 cc/kg and PP <30
What is regional over-distension in ARDS
preset volume modes
air flows into most complaint alveoli
causes some alveoli to be over distended and others to be underinflated
What is the problem with AC ventilation in ARDS
regional over-distension in ARDS
what can happen with regional overdistension in ARDS
alveolar wall trauma and cellular injury
can increase atelectasis
can cause pneumothorax
What should you keep tidal volumes in ARDS pts
btwn 4-8 ml/Kg
What is permissive hypercapnia? why is it a protective lung strategy
allowing pCO2 to rise with low tidal volumes
preferable not to drop pH below 7.2
avoids volume and barotrauma that might come from increasing PCV to increase ventilation
why do we not increase RR to blow off rising pCO2
decreased time for resp cycle
cases increased flow rate d/t dec. in inspiration time
lung tissue has less time to stretch and accommodate incoming volume
increases airway and alveolar pressure
If your TV is decreaseing what are 4 things this could mean
decreased lung compliance
worsening ARDS
secretions need suctioning
leak in circuit
T or F volume-cycled ventilation decreases the risk of volutrama and barotrauma
false - PC reduces risk of barotrauma and volutrauma
3 benefits of PC
improve ventilation d/t decelerating inspiratory flow pattern
laminar flow opens smaller collapsed airways
improve oxygenation by decreasing V/Q mismatch
what can we do with MV to improve refractory hypoxemia
increase PEEP sometimes as high as 15-18
keep FiO2 levels as low to prevent alveolar damage from O2 toxicity
What are the two types of ECMO
VA
VV
what type of ECMO provides cardiac support to assist systemic circulation
VA
What type of cannulation does VA require? VV?
VA - arterial and venous
VV - venous only
What type of ECMO bypasses pulmonary circulation
VA
what type of ECMO maintains pulmonary blood flow
VV
What type of ECMO would you use for RV failure
VA
Which type of ecmo acheives a higher PaO2
VA
What type of ECMO is connected in series to heart and lungs? parallel to heart and lungs?
VV series to heart and lungs
VA parallel to heart and lungs
what are our two hemodynamic goals in ARDS
maintain preload
avoid excessive fluid
what type of fluid management do we do with ARDS pt
biphasic
hemodynamic instability - early fluid administration
once initial phase of instability has passed then restrictive fluid strategies
what type of fluid do we use with ARDS
remains isotonic crystalloid
what is normal PAS/PAD
20-30/10-15
what is normal PCWP
8-12
what is normal SVR
800-1500
What is normal PVR
155-255
what is normal CO
4-8
What should the difference btween PCWP and PAD be
1-4 mmHg
if there is difference >4mmHg btw PCWP and PAD what does this indicate
lung pathology
what is something we can get for our ARDS pts that maximizes ventilation and perfusion
kientic bed
what does a kinetic bed do
constant repositioning maximizes ventilation and perfusion improving gas exchange
What position is beneficial in ARDS pts? why?
proning
improves lung persusion in dependent lung zones
how long should ARDS pts be placed in the prone position
12-16 horus
how many people does it take to prone a pt
3-4 RNS and one RT
what are 3 side effects of proning a pt
potential tube or line dislodgement
pressure wounds, pressure neuropathy
facial edema
What RASS goal do we typically aim for with ARDS pts
-3 to -5
why do we want ARDS pts sedated
decrease demand
easier to ventilate
promote patient comfort while on ventilator
What type of drugs do we expect to use with ARDS pts
bronchodilators
mucolytics
have surfactant replacement drugs shown benefit in ARDS pts
no
what mediaction might be used as a last effort to imrpove oxygenation for ARDS pts
nitric oxide
what does nitric oxide do
vasodilation of capillary bed reduces PVR improves blood flow reduces V/Q mismatch decreases O2 toxicity decrease high PEEP requirements
What are 2 side effects of nitric oxide
interacts with Hgb to form methemoglobin
can cause renal dysfunction
late stage blood gas for ARDS will show what
mixed acidosis
What PA values will be abnormal in ARDS
decreased SVR d/t to ABCCs of inflammation increased PVR (increased RT sided afterload) increased PAD (left sided preload)
if you have high PCWP and PADP greater than 4 what does this indicate
HF
will PCWP be affected in ARDS
no
if you hear bronchial breath sounds in the lower and mid lung fields what does this mean
consolidation happening in the lungs
what happens during alveolar epithelial changes
type 1 cells wall integrity compromised causing shift in fluid and protein
type 2 cell damage causes loss of surfactant
What happens to O2 supply and demand during alveolar epithelial changes
decreased SA
thickened membrane
decreased diffusion and decreased alveolar oxygenation
what TV do you expect to see for decreased mortality in ARDS pts? PP?
<6 cc/Kg
<30 cm
What type of pt must you be mindful of with permissive hypercapnia
TBI
high CO2 causes cerebral vasodilation which can cause increased ICP
what vent settings places a pt at risk for regional overdistention
volume cycled, AC
why do you want to avoid excessive fluid resuscitation in ARDS pts
dont want to overload them and cause more fluid to back up into the lungs
what type of blood gas will you see in a patient who is being diuresed with lasxi
metabolic alkalosis
how should you be giving fluids in patients
slowly and carefully as pt already has fluid in the lungs
What is the main thing positioning addresses
V/Q mismatch
what are benefits to proning
expands alveoli as heart is not pushing down on them as seen in supine
allows for better oxygenation of dependent side of lung as the fluid will move via gravity
what are the two types of patients you will never do a sedation vacation on
ARDS
TBI
what is another drug that can be used aside from nitric oxide in ARDS pts
flolan (prostacylcin)
how do flolan work
used in pulmonary htn to vasodilate pulmonary arteries
cheaper than nitric oxide
