Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

7520 Final > ARDS > Flashcards

ARDS Flashcards

1
Q

the following points best describes ARDS

A
  • can cause severe hypoxemia that can be resistant to O2 therapy
  • involves noncardiogenic cardio pulm edema
  • decreases lung compliance
  • characteristic CXR changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is an example of an ARDS direct insult?

A

pneumonia, aspiration, pulm contusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

An indirect insult for ARDS?

A
  • sepsis, severe pancreatitis, shock states
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what happens in sepsis and SIRS

ARDS?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Berlin def of ARDS

A
  1. timing: within 1 week of a known clinical insult of new or worsening resp symptoms
  2. chest imaging- bilateral opacities, not fully explained by effusions, lobar/lung collapse, or nodules
  3. Origin of Edema- resp failure not explained by cardiac failure or fluid overload. Need to exclude hydrostatic edema if no risk factor present
  4. Oxygenation- P/F ratio
    PaO2/FiO2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

P/F ration ranges

A

mild 200-300

moderate 200-100

severe < 100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

P/F ratio data

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

the effects of ARDS can be seen in PA line values in which of the following ways?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Plateau Pressure

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

PIP/Ppeak

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

protective airway strategies

A

an approach to mech vent in which the aim is to limit vent-associated lung injury

  1. maintain airway plateau pressures < 30
  2. use of low tidal volumes
  3. permissive hypercapnia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

considerations when using pressure Control Vent in ARDS

A
  • 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?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Refractory Hypoxemia

A
  • is a hallmark of ARDS
  • hypoxemia that doesnt improve with increases in supplemental O2
  • it is caused by impaired diffusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

physiological process most commonly associated with refractory hypoxemia include

A

severe V/Q mismatch - Shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pathophysiologic process that contributes most strongly to refractory hypoxemia include

A

significantly impaired diffusion

** It is caused by imared diffusion**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Biphasic fluid replacement

A

-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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what happens to BP from PEEP

A

BP can drop from an increase in PEEP from increased intrathoracic pressure which reduces preload, can lead to decreased contractility and decreased CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ARDS is triggered from?

A

SIRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

SIRS clinical presentation

A
  1. severe vasodilation = relative hypovolemia
  2. increased capillary permeability = fluid shift and further hypovolemia
  3. selected areas of innaprop vasoconstriction, with vasodilate = maldistribution of blood flow
  4. depression of myocardial contractility (when SIRS severe and is direct result of myocardial depressant factor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

inflam response

A

Arachidonic, bradykinin, coagulation, compliment

vasodilate, increased permiability, microemboli, damage to endothel = cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ards patho

phase 1

A

Injury/insult to capillary or alveolus. reduces blood flow and precipitates chemical mediator release (histamine, serotonin, bradykinin)

  • increased permeability and vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Phase 2

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Phase 3

A

Exudative
- pulm edema

  • Type 1 cells die
  • compression of alveoli and small airways

= Oxygenation issue, diffusion and V/Q mismatch prob = Shunt!

24
Q

Phase 4

A

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

25
Q

Phase 5

A

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)

26
Q

Phase 6

A

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

27
Q

Pulm edema causes (O2 framework)

A

(interstitial edema)
- vent: decreased lung compliance

  • oxygenation: decreased Surface area, thickened A-C mem*, shunt = diffusion
28
Q

Microemboli causes

A

oxygenation: dead space

CO: Right ventricle failure

29
Q

Fibrosis

A

vent: decreased lung compliance

Oxygenation: thick A-C membrane

O2 demand: increased WOB

30
Q

Type 1 cell death

A

vent: increased PaCO2

Oxygenation: decreased PaO2

31
Q

Type 2 cell death

A

vent: loss of surfactant

O2 demand: increased WOB

32
Q

Alveoli compression

A

vent: decreased FRC

Oxygenation: decreased surface area?

33
Q

Interstitial space

A

thickened A-C

34
Q

pulm edema

A
  • shunt/shunt-like
  • dec surface area
  • dec compliance
35
Q

Alveoli compressed/collapsed

A
  • dec surface area
  • dec resistance
  • dec FRC
  • dec compliance
  • dec vol
  • inc demand (WOB, anxiety)
36
Q

loss of surfactant

A
  • dec compliance
  • dec vol
  • inc demand (WOB)
37
Q

capillary damage and microemboli

A
  • dead-like
  • inc Right vent afterload
  • worsening PA pressures
38
Q

Progressive fibrosis and protein layer

A
  • thick A-C
  • dec compliance
  • dec vol
  • inc demand (WOB)
39
Q

signs of cardiogenic edema

A
  • 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
40
Q

what does PAD/PCWP and SVR look like in HF vs ARDS

A

HF
PAD/PCWP: 20, 15
SVR: 1550

ARDS
PAD/PCWP: 20, 10
SVR: 600

41
Q

PAD measures?

influenced by?

A

Left Preload

  • blood flow and vascular tone
42
Q

PCWP measures?

influenced by?

A

left preload

-blood flow and vascular tone

43
Q

ARDS management

A

treat the cause and supportive management

  • protective lung
  • optimize gas exchange
  • fluid therapy
  • pharmacology
44
Q

what are protective lung strategies

A
  • tidal vol < 6cc/kg
  • plat pressure < 30
  • permissive hypercapnia
45
Q

how do we cause volutrauma? barotrauma?

A

vol- from high tidal volumes

baro- from high pressure

46
Q

when we set Pressure control?

A
  • 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)
47
Q

PC pressure

A
  • distribution of gas better than AC. Will not over distend alveoli.
  • laminar flow
48
Q

permissive hypercapnia

A

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)

49
Q

do not use permissive hypercap on PTs who are…

A
  • have high ICP

- seizures

50
Q

what is the new goal for permissive hypercap and why?

A

7.20, below that vasoactive drugs dont respond well

51
Q

supportive management

A
  1. optimize gas exchange

2. support diffusion

52
Q

how do you support V/Q matching (gas exchange)

A

1, Recruit alveoli - vent settings, Peep, recruit maneuvers

  1. Prevent alveoli collapse: peep
  2. suction- when necessary to prevent shunt-like airway by removing secretions
  3. optimize CO
  4. Positioning. kinetic bed
  5. prone
53
Q

Optimizing Diffusion

A
  1. PEEP- thins the A-C, decrease WOB, prevent alveoli collapse, allow more time for gas exchange (FRC)
  2. FiO2- the most min required
54
Q

what types of pharmacology is needed

A
  1. to decrease O2 demand
  2. Tolerate the vent
  3. bronchodilators (and mucolytics)
  4. pulm vasodilators
  • fever control
  • analgesia
  • sedatives
  • NMBA
  • RASS goal?
55
Q

what is nitric oxide used for?

A

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
56
Q

side effect of nitric oxide

A
  • interacts with Hgb forming methylhemoglobin which impares the release of O2 at the cellular level
57
Q

flolan- epoprostenol does what?

implications?

A
  • 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

7520 Final (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions