ARDS Flashcards
the following points best describes ARDS
- can cause severe hypoxemia that can be resistant to O2 therapy
- involves noncardiogenic cardio pulm edema
- decreases lung compliance
- characteristic CXR changes
what is an example of an ARDS direct insult?
pneumonia, aspiration, pulm contusion
An indirect insult for ARDS?
- sepsis, severe pancreatitis, shock states
what happens in sepsis and SIRS
ARDS?
the normal inflam and immune response gets out of control (dysregulated) and begins to exert its effects systemically
- inflam goes from local to systemic
- ARDS happens when this out of control inflam response occurs in the lungs
Berlin def of ARDS
- timing: within 1 week of a known clinical insult of new or worsening resp symptoms
- chest imaging- bilateral opacities, not fully explained by effusions, lobar/lung collapse, or nodules
- Origin of Edema- resp failure not explained by cardiac failure or fluid overload. Need to exclude hydrostatic edema if no risk factor present
- Oxygenation- P/F ratio
PaO2/FiO2
P/F ration ranges
mild 200-300
moderate 200-100
severe < 100
P/F ratio data
- you require an ABG to calculate it
- it represents the difference between the amount of O2 in the alveoli and the amount dissolved in the plasma
- If the PT was on RA it would be 21%
- this tool helps us quantify pulm shunting
the effects of ARDS can be seen in PA line values in which of the following ways?
- PAS and PAD rise in the presence of ARDS
- A difference greater than 4 between the PAD and PCWP suggests the PT is experiencing significant pulm changes
- PA cath’s dont diagnose ARDs but
- you can bypass influences and get a better view of the left vent when obtaining a PCWP pressure
- PAD is supposed to be slightly higher then the wedge, but > 4 = poss ARDS
Plateau Pressure
is measured at the end of inspiration in the absence of any air flow through the system.
This measures only the compliance of the lungs (static compliance)
- measured at the end of full inspiration “inspiratory hold” -this stops the flow of gas and hence eliminates pressures created by airway and circuit resistance
- mntn < 30
PIP/Ppeak
peak inspiratory pressure is a product of the rate of flow of air through the vent tubing and airway. the diameter of the airway and the lung compliance
- influenced by tidal vol, lung compliance, airway resistance, vent circuit resistance
- this is dynamic lung compliance
protective airway strategies
an approach to mech vent in which the aim is to limit vent-associated lung injury
- maintain airway plateau pressures < 30
- use of low tidal volumes
- permissive hypercapnia
considerations when using pressure Control Vent in ARDS
- there is laminar flow, which lowers the airway pressure and assists in opening the smaller collapsed airways, thus minimizing tidal vol delivery with each breath
- there is no set vol
- Tidal vol is monitored on an hourly basis bc a decreasing Tv will indicate important changes in Pt condition
- -> do they need suctioning?
- -> is there compliance worsening?
Refractory Hypoxemia
- is a hallmark of ARDS
- hypoxemia that doesnt improve with increases in supplemental O2
- it is caused by impaired diffusion
physiological process most commonly associated with refractory hypoxemia include
severe V/Q mismatch - Shunt
Pathophysiologic process that contributes most strongly to refractory hypoxemia include
significantly impaired diffusion
** It is caused by imared diffusion**
Biphasic fluid replacement
-biphasic fluid replacement is recommended: in initial phase, early adequate fluid administration as required to restore hemodynamic stability. Once more stable, restrictive fluid strategies are followed. Goal: maintain lowest preload compatible with adequate CO and O2 delivery
what happens to BP from PEEP
BP can drop from an increase in PEEP from increased intrathoracic pressure which reduces preload, can lead to decreased contractility and decreased CO
ARDS is triggered from?
SIRS
SIRS clinical presentation
- severe vasodilation = relative hypovolemia
- increased capillary permeability = fluid shift and further hypovolemia
- selected areas of innaprop vasoconstriction, with vasodilate = maldistribution of blood flow
- depression of myocardial contractility (when SIRS severe and is direct result of myocardial depressant factor)
inflam response
Arachidonic, bradykinin, coagulation, compliment
vasodilate, increased permiability, microemboli, damage to endothel = cell death
Ards patho
phase 1
Injury/insult to capillary or alveolus. reduces blood flow and precipitates chemical mediator release (histamine, serotonin, bradykinin)
- increased permeability and vasodilation
Phase 2
Exudative Phase
chemical mediators of inflammation= increased alveolar capillary membrane permeability; fluid shift to interstitial space
- injury to pulm capillaries
- increased A-C mem permeability
- leak fluid: protein, blood cells, fibrin to interstitial space
- microemboli formation
= V/Q mismatch and dead spaces
Phase 3
Exudative
- pulm edema
- Type 1 cells die
- compression of alveoli and small airways
= Oxygenation issue, diffusion and V/Q mismatch prob = Shunt!
Phase 4
Proliferative
- Type 2 alveolar cells distroyed
- decreased surfactant production = impaired diffusion and decresaed compliance = increased WOB and increased demand
V/Q mismatch = cant participate in gas exchange
Phase 5
Proliferative phase
- alveoli start to collapse
- oxygenation severly impaired
- CO2 is still able to be removed bc of diffusion coefficient
Type 1 respiratory failure (decreased O2, Type 2 is increased CO2)
Phase 6
Fibrotic phase
-alveoli become enlarged and irregularly shaped (fibrotic)
- pulm capillaries become scarred
- = continued stiffening of the lungs increasing pulm HTN and continued hypoxia
scarring effects CO = increased Pulm artery pressure and Right sided HF
Pulm edema causes (O2 framework)
(interstitial edema)
- vent: decreased lung compliance
- oxygenation: decreased Surface area, thickened A-C mem*, shunt = diffusion
Microemboli causes
oxygenation: dead space
CO: Right ventricle failure
Fibrosis
vent: decreased lung compliance
Oxygenation: thick A-C membrane
O2 demand: increased WOB
Type 1 cell death
vent: increased PaCO2
Oxygenation: decreased PaO2
Type 2 cell death
vent: loss of surfactant
O2 demand: increased WOB
Alveoli compression
vent: decreased FRC
Oxygenation: decreased surface area?
Interstitial space
thickened A-C
pulm edema
- shunt/shunt-like
- dec surface area
- dec compliance
Alveoli compressed/collapsed
- dec surface area
- dec resistance
- dec FRC
- dec compliance
- dec vol
- inc demand (WOB, anxiety)
loss of surfactant
- dec compliance
- dec vol
- inc demand (WOB)
capillary damage and microemboli
- dead-like
- inc Right vent afterload
- worsening PA pressures
Progressive fibrosis and protein layer
- thick A-C
- dec compliance
- dec vol
- inc demand (WOB)
signs of cardiogenic edema
- S3, 4
- murmur, elevated JVD, cardiomeg
- elevated BNP (with other data)
- TEE/TTE: poor EF, valve dysfunction, severe diastolic dysfunction
- assess fluid statue: echo, bedside US, PA cath
what does PAD/PCWP and SVR look like in HF vs ARDS
HF
PAD/PCWP: 20, 15
SVR: 1550
ARDS
PAD/PCWP: 20, 10
SVR: 600
PAD measures?
influenced by?
Left Preload
- blood flow and vascular tone
PCWP measures?
influenced by?
left preload
-blood flow and vascular tone
ARDS management
treat the cause and supportive management
- protective lung
- optimize gas exchange
- fluid therapy
- pharmacology
what are protective lung strategies
- tidal vol < 6cc/kg
- plat pressure < 30
- permissive hypercapnia
how do we cause volutrauma? barotrauma?
vol- from high tidal volumes
baro- from high pressure
when we set Pressure control?
- for dec lung compliance
- min risk trauma
- we set: pressure, RR, PEEP
- time and PT triggered
- time cycles (1 sec insp)
- provides both controlled and assist (Pt triggers breath but the rest of the breath is controlled by vent)
PC pressure
- distribution of gas better than AC. Will not over distend alveoli.
- laminar flow
permissive hypercapnia
if we dont have room to increase minute vol = RR x TV
then we allow the CO2 to rise to decrease the risk of vol/barotrauma and auto-peep (when airflow doesnt return to zero at end exhale)
do not use permissive hypercap on PTs who are…
- have high ICP
- seizures
what is the new goal for permissive hypercap and why?
7.20, below that vasoactive drugs dont respond well
supportive management
- optimize gas exchange
2. support diffusion
how do you support V/Q matching (gas exchange)
1, Recruit alveoli - vent settings, Peep, recruit maneuvers
- Prevent alveoli collapse: peep
- suction- when necessary to prevent shunt-like airway by removing secretions
- optimize CO
- Positioning. kinetic bed
- prone
Optimizing Diffusion
- PEEP- thins the A-C, decrease WOB, prevent alveoli collapse, allow more time for gas exchange (FRC)
- FiO2- the most min required
what types of pharmacology is needed
- to decrease O2 demand
- Tolerate the vent
- bronchodilators (and mucolytics)
- pulm vasodilators
- fever control
- analgesia
- sedatives
- NMBA
- RASS goal?
what is nitric oxide used for?
Flolan
- inhaled vasodilator as rescue therapy to improve oxygenation and allow time to implement other things
- acts on endothelium of capillary bed without causing systemic vasodilation
- reduces PVR, improves blood flow, and reduces V/Q mismatch
- improves gas exchange by enhancing blood flow to ventilated areas of the lungs
side effect of nitric oxide
- interacts with Hgb forming methylhemoglobin which impares the release of O2 at the cellular level
flolan- epoprostenol does what?
implications?
- vasodilate pulm and systemic arterial vascular
- inhibit platelet aggregation
- short 1/2 life
- can cause bleeding
- sudden withdrawal can cause rebound HTN
- stable at RA for 8 hrs then needs ice packs
