Brainscape's Knowledge GenomeTM

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


See full index

MDRS > ARDS > Flashcards

ARDS Flashcards

1
Q

What is ARDS

A
  1. acute diffuse, inflammatory lung
    injury –> increased pulmonary
    vascular permeability,

2.hypoxemia and bilateral radiographic
opacities, associated with increased venous

  1. increase deadspace
  2. decrease lung compliancce
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

timing of ARDS

A

Acute: onset of DX must be with
in 1 week of a known clinical insult or
new/worsening respiratory symptoms (most cases occur within 72

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

ARDS in cxr?

A

Bilateral opacities consistent with pulmonary edema

–> not fully explained by
effusions, lobar/lung collapse or nodules

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

what is the origin of edema

A

not caused by cardiogenic or fluid overload

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

what are the classification of ARDS?

A

Mild 27%
Moderate 32%
Severe 45%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the dx of mild ARDS

A

200

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

What is the dx of moderate ARDS

A

100

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

What is the dx of severe ARDS

A

PaO2/FiO2 <100

With PEEP ≥ 10cmH2O

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

how to detect bilateral opacities?

A

CXR

CT

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

what cause ARDS

A

Acute processes that directly or indirectly
cause injury to the respiratory epithelium and endothelium of the pulmonary
capillaries;

–>->increasing permeability of capillaries and
causing alveolar flooding.

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

.direct injury that cause ARDS

A 
pneumonia
gastric aspiration 
near-drowning
lung contusion
toxic inhalation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

indirect injury that cause ARDS

A

sepsis
burn
sickle cell crisis
prolonged systemic hypotension and shock

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

What are the 2 phases on ARDS injury

A

Exudative phase: day 1 - 3

  • Endothelial (capillary) damage
  • ->Good outcomes if recovery after this phase

Fibro proliferative phase: day 3-7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the pathophysiology of ARDS

A
  1. Clinical lung injury
  2. Endothelial damage (exudative phase )
  3. Platelet aggregation
  4. Release of neutrophil chemotactic factors
  5. Neutrophil aggregation and release of mediators which causes vasoconstriction
  6. Alv cap. membrane permeability
    (damage to type 1 pneumocytes
  7. Exudation of fluid, protein, RBC’s into interstitium
    8.V/Q mismatching
  8. Acute Respiratory Failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does hyaline membrane formation lead to

A

Fibrosis causing severe impairment of ventilation

, then lead to ARDS

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

what are the Major Pathologic Changes

A
  • Decreased surfactant
  • -> atelectasis, decrease compliance
  • ->increase WOB, dyspnea
  • Increased alveolar capillary membrane permeability
  • –>pulmonary edema
  • Vasoconstriction (HPV)
  • –>V/Q mismatch
17
Q

what are the Progressive clinical presentation

A 
Hyperventilation
Respiratory alkalosis
Dyspnea &amp; hypoxemia
Respiratory &amp; metabolic acidosis
Refractory hypoxemia
Decreased cardiac output
Hypotension --> decrease perfusion 
\+/
MODS
death
18
Q

what can rule out a cardiogenic origin of pulmonary edema?

A

PCWP <18mmhg

19
Q

what are the s&s of ARDS in the first 24- 48 hours?

A
  • hyperventilation
  • anxiety
  • tachycardia
  • CXR normal

ABG
hypoxemia

20
Q

what are the Anatomic Alterations of the Lungs

A 
- Interstitial and intra alveolar edema and
hemorrhage
- Alveolar consolidation
- Intra alveolar hyaline membrane
- Pulmonary surfactant deficiency or
abnormality
- Atelectasis
21
Q

Is pulmonary edema in ARDS result of hydrostatic or non-hydrostatic

A

Non-hydrostatic

22
Q

what are the characteristics of hydrostatic pulmonary edema

A

Flooding occurs in “all or nothing” manner

Fluid filling alveoli is identical to interstitial fluid

23
Q

wat does Non-hydrostatic mean and characteristics

A

Fluid accumulates despite normal hydrostatic
pressure

DUE TO INFLAMMATION
Vascular endothelial injury alters permeability
Protein rich fluid floods interstitial space
Alveolar flooding occurs as osmotic pressures in
capillaries & interstitium equalize
Alveolar epithelium & pulmonary fluid clearance are
impaired

24
Q

what is the result of gas exchange during ARDS

A

Restrictive physiology & refractory hypoxemia

low lung compliance due to fibrosis and edema

V/Q mismatch

25
Q

How to differentiate between CHF and ARDS

A

CHF: cardiomegaly, perihilar infiltrates, pleural
effusions

ARDS: peripheral alveolar infiltrates, air
bronchograms, sparing of costophrenic angles, &
normal cardiac size

26
Q

what may create a false positive on a reading of CHF

A

Carefully appraise results as catheter placement

may reflect high PEEP or P aw instead of PCWP

27
Q

what is shown in Bronchoalveolar lavage fluid (BALF) in ARDS

A
  • contain large amounts of inflammatory cells
28
Q

What is the general management for ARDS

A

nitric oxide (bottom line: $ yet no effect on
patient positioning (prone)
exogenous surfactant (?)
PA catheter (Swan Ganz)
diuretic agents, corticosteroids, antibiotics
ECMO (Extracorporeal membrane oxygenation)

29
Q

how to offset atelectasis in ARDS

A

PEEP and/or CPAP

30
Q

what are the goals of Therapeutic Goals of Low

Tidal Volume Ventilation

A
  1. Decrease high transpulmonary pressure
  2. Reduce overdistention of the lungs
  3. Decrease barotrauma
31
Q

what are the complicatoin of ARDS

A

VILI - ventilator induced lung injury

MOD - multiple organ dysfunction syndrome

32
Q

when is corticosteriod used?

A

high doses are used for late, uncomplicated pulmonary
fibrosis following ARDS study showed improved gas
exchange & low mortality

33
Q

when is corticosteriod not used?

A

routine use, and giving it early
cannot be advocated & should
be strictly avoided after 14 days
from onset of symptoms

MDRS (23 decks)

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