ARDS Flashcards
(57 cards)
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
