Brainscape's Knowledge GenomeTM

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


See full index

(HGC) ACNP804 Exam 4 > ARDS (Various PDFs, Harrisons) > Flashcards

ARDS (Various PDFs, Harrisons) Flashcards

1
Q

When was ARDS first recognized?

A

World War I, when it was recognized that some patients with non-thoracic injuries developed respiratory distress, diffuse lung infiltrates, & respiratory failure.

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

Jeopardy style!

The most severe form of acute lung injury, a form of diffuse alveolar injury.

A

What is acute respiratory distress syndrome, or ARDS?

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

In ARDS, the PaO2/FIO2 ratio is less than…

A

200

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

In ALI (acute lung injury), the PaO2/FIO2 ratio is less than…

A

300

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

For ARDS to be diagnosed, what other condition must be excluded? How do you exclude it?

A

Cardiogenic pulmonary edema; by clinical criteria or by pulmonary capillary wedge pressure < 18

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

Which phase of ARDS is exudative?

A

Early

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

Which phase of ARDS is fibroproliferative?

A

Late

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

The site of injury in ARDS may be either…

A

1) the vascular endothelium (as in sepsis)

2) the alveolar epithelium (as in aspiration of gastric contents)

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

2 types of alveolar epithelial cells

A

Type I & Type II

Oooh that was hard

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

Describe Type I alveolar epithelial cells

A

1) Make up 90% of the alveolar epithelium
2) Easily injured
3) Damage allows increased entry & decreased clearance of fluid into alveoli

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

Describe Type II alveolar epithelial cells

A

1) Fewer of them
2) More resistant to injury
3) Functions include: production of surfactant, ion transport, proliferation & differentiation into Type I cells after cellular injury (repair processes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is it so much worse if Type II alveolar cells are damaged?

A

BECAUSE THEY’RE IMPORTANT!

Decreased surfactant results in decreased compliance & alveolar collapse, then interference with the normal repair process leads to fibrosis.

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

Neutrophils in ARDS

A

Thought to play a key role, but may be reactive rather than causative

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

Cytokines in ARDS

A

Imbalance of proinflammatory & anti-inflammatory cytokines thought to occur after inciting event.

Can happen because of positive pressure ventilation: ventilator-associated lung injury (VALI)

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

ARDS causes a marked increase in __________ (2 words), leading to severe hypoxemia.

A

intrapulmonary shunting

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

What’s the association between pulmonary hypertension & ARDS

A

You will see pulmonary hypertension in ARDS patient. It normalizes as the syndrome resolves.

Pulmonary artery vasoconstriction likely contributes to ventilation-perfusion mismatch, leading to hypoxemia.

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

ARDS resolution?

A

The acute phase usually resolves completely.

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

If the acute phase of ARDS doesn’t resolve completely, what do we end up with?

A

Residual pulmonary fibrosis.

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

How can we check for progression to fibrosis?

A

1) Increased levels of procollagen peptide III early in the course (in the fluid found by bronchioalveolar lavage)
2) Fibrosis findings upon biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

The indicators or findings of fibrosis correlate with…

A

…an increased mortality rate.

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

What percentage of ARDS patients have no identified risk factors?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the most common risk factor for ARDS?

A

Sepsis

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

Risk factors for ARDS generally fall into these 3 categories:

A

1) Direct lung injury (as in aspiration)
2) Systemic illnesses
3) Injuries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Major risk factors associated with ARDS

A 
#Bacteremia & sepsis
#Trauma (with or without pulmonary contusion)
#Fractures (particularly multiple or long bone)
#Burns
#Massive transfusion
#Pneumonia
#Aspiration
#Drug overdose
#Near drowning
#Postperfusion injury after bypass
#Pancreatitis
#Fat embolism
#Metabolic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Factors that increase the risk of ARDS after inciting event:

A 
#Advanced age
#Female sex (only in trauma)
#Smoking
#Alcohol use
26
Q

As severity of illness increases (as gauged by a severity scoring system such as APACHE), what happens to risk for ARDS?

A

It increases!

The sicker you are, the sicker you’re likely to get! SURPRISE!

27
Q

True or false: Most deaths in ARDS patients are attributable to primary pulmonary cause.

A

False. Most are attributable to sepsis or multi-organ failure.

28
Q

Which is a better indicator of prognosis: PaO2/FIO2 ratio at the time of diagnosis, or lack of pulmonary improvement in the first week?

A

The PaO2/FIO2 ratio does not correlate with outcome, but the lack of improvement within the first week is a poor prognostic factor.

29
Q

So how long does it take to get over ARDS entirely?

A 
A freaking long time. ARDS patients have 
#prolonged hospital courses
#frequent nosocomial infections (like VAP)
#Functional impairment for months & years post-recovery
#Decreased health-related quality of life (HRQL) compared to general population.
#In short: ARDS SUCKS BAD.
30
Q

Harrison’s defines ARDS as…

A

“a clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse pulmonary infiltrates leading to respiratory failure.”

31
Q

Important ratio in the diagnosis of ARDS & ALI:

A

FiO2 (percentage of inspired O2)

32
Q

What percentage of ICU admissions have acute respiratory failure? What percentage of those patients meet criteria for ALI or ARDS?

A

10% of all ICU admits

20% of those meet ALI/ARDS criteria

33
Q

When a patient is suffering from more than 1 of the ARDS- predisposing conditions, what happens to risk?

A

Goes up, of course!

So if I have trauma, I might get ARDS, but if I have trauma AND sepsis, I’m way more likely. HOW NICE FOR ME.

34
Q

ARDS pathophysiology happens in 3 phases:

A

1) Exudative
2) Proliferative
3) Fibrotic

35
Q

Exudative phase characteristics

A

Type I pneumocytes (alveolar epithelial cells) are injured&raquo_space;
Loss of alveolar barrier&raquo_space;
Edema fluid accumulates in interstitial/alveolar spaces&raquo_space;
Cytokines & lipid mediators are present&raquo_space;
Neutrophils go into interstitium & alveoli&raquo_space;
Vascular obliteration by microthrombi & fibrocellular proliferation

36
Q

On an AP CXR, the exudative phase of ARDS can be easily confused with what other condition?

A

The pulmonary congestion of left heart failure!

37
Q

The alveolar edema of the exudative phase usually involves what part of the lung?

A

Dependent portions, leading to diminished aeration & atelectasis

38
Q

When large parts of dependent lungs collapse, this decreases lung compliance. What happens next?

A

Intrapulmonary shunting & hypoxemia, leading to increased work of breathing and dyspnea.

39
Q

Microvascular occlusions lead to…

A

…reduction in pulmonary arterial blood flow to the portions of lung that ARE ventilated, further increasing dead space and causing pulmonary hypertension and thus, hypercapnia.

40
Q

ARDS (exudative phase) in a nutshell

A

1) Injury of Type I pneumocytes, then
2) Edema fluid enters alveoli, then
3) Alveoli collapse, especially in dependent portions of lung, then
4) Lung compliance is decreased, then
5) Intrapulmonary shunting & hypoxemia increase the work of breathing (so, dyspnea), while
6) Occlusions in microvasculature reduce pulmonary arterial flow, leading to pulmonary hypertension, which causes
7) Hypercapnia

TADA, YOU’RE A PRO!

41
Q

When does the exudative phase happen?

A

The first 7 days after exposure to risk factor.

Usually 12-36 hours, but can be up to 5-7 days.

42
Q

What does it look like clinically?

A 
#Dyspnea with rapid, shallow breathing & air hunger
#Tachypnea leading to fatigue & respiratory failure
#CXR show interstitial opacities
#CXR looks like cardiogenic pulmonary edema (to differentiate, ARDS rarely shows cardiomegaly, pleural effusions, or pulmonary vascular redistribution)
#CT: heterogeneity of lung involvement (remember: look for dependent atelectasis)
43
Q

What are some differentials for the exudative phase of ARDS?

A 
COMMON:
#Cardiogenic pulmonary edema
#Diffuse pneumonia
#Alveolar hemmorhage
LESS COMMON:
#Acute interstitial lung diseases
#Acute immunologic injury
#Toxins
#Neurogenic pulmonary edema
44
Q

When does the proliferative phase of ARDS happen?

A

About days 7 to 21

45
Q

ARDS (proliferative phase) in a nutshell:

A

1) Shift from neutrophil to lymphocyte pulmonary infiltrate and
2) Proliferation of Type II pneumocytes, which synthesize new surfactant & differentiate into Type II pneumocytes, which is basically
3) Initiation of lung repair

Most peeps recover rapidly & get to come off the vent during this phase. SCORE! We fixed it!

46
Q

But if a patient in the proliferative phase has procollagen peptide, they may enter what phase? Why’s that bad?

A

Fibrotic phase dramatic music, which is associated with a longer clinical course & increased mortality. BOOOOO.

47
Q

ARDS (fibrotic phase) in a nutshell:

A

1) Edema & exudates convert to alveolar & interstitial fibrosis, which
2) Disrupts acinar architecture, leading to
3) Emphysema-like changes with large bullae while
4) Fibroproliferation in microcirculation leads to progressive occlusion & pulmonary hypertension

Consequences: increased risk of pneumothorax, reduced lung compliance, increased dead space, and potentially long-term ventilator support. NOOOOO. We didn’t fix it. :(

48
Q

We’ve recently reduced ARDS, but mostly because we got better at treating critically ill people in general. So, we should pay close attention to:

A

1) Treatment of the underlying conditions & disorders
2) Minimizing procedures/complications
3) Prophylaxis for VTE, GI bleeding, aspiration, sedation, & central line infections
4) Recognition of nosocomial infections
5) Adequate nutrition

49
Q

For your ARDS patient: high or low tidal volume?

A

LOOOOOOOW!

Attempts to full inflate the collapsed dependent part of the lung may overdistend the normal, less involved portions, leading to injury.

50
Q

Ventilator-induced lung injury requires 2 processes. What are they?

A

1) Repeated alveolar overdistention
2) Repeated alveolar collapse

Basically your alveoli were not meant to do jumping jacks, & they don’t handle it very well.

51
Q

Our biggest advance to date in ARDS mortality:

A

Figuring out that lower tidal volumes in mechanical ventilation meant lower mortality rates.

In the study cited: low (6 mL/kg) vs high (12 mL/kg) ventilation. Mortality in low volume patients was 31%, but 40% in high volume patients.

52
Q

What does PEEP stand for in the context of mechanical ventilation?

A

Positive end-expiratory pressure

53
Q

Okay, so what does PEEP mean?

A

It’s the pressure required to keep alveoli from collapsing at the end of expiration

54
Q

At what pressure should we set the PEEP?

A

Empirically to minimize FiO2 and maximize PaO2.

55
Q

What’s “proning?” Why would we do it?

A

Proning: mechanical ventilation in the prone position

It has improved arterial oxygenation in randomized trials

56
Q

If it’s so great, why would we NOT want to “prone” our ARDS patients?

A

Effect on outcomes is still uncertain, and unless your ICU team is trained & experienced in this positioning, you could screw up any number of things: lose the ET tube, pull out the CVLs, break the patient…y’know. That sort of thing.

It’s still a last-ditch effort until we know more about whether it works.

57
Q

Some adjunctive ventilator therapies to be aware of:

A 
#high PEEP
#Inverse ratio ventilation (I:E > 1:1)
#Recruitment maneuvers
#Prone positioning
#High frequency ventilation (extremely high resp rates of 5-20 cycles per second) with low tidal volumes
#Partial liquid ventilation (promising preliminary data)
#ECMO (extracorporeal membrane oxygenation) which has clear survival benefit in neonates; maybe some utility in certain adults

There is no evidence that these benefit survival as of yet.

58
Q

How should we manage fluid in ARDS patients? Why?

A

Aggressively manage fluid with restrictions & diuretics to keep left atrial filling pressures low, minimizing pulmonary edema.

Benefits: prevents further decreases in lung compliance, improves pulmonary mechanics, shortens ICU stay, decreases mortality! Good times all around.

JUST DON’T HYPOPERFUSE THE KIDNEYS. They’re drama queens.

59
Q

Glucocorticoids in ARDS: yes or no

A

Nope. We tried it in some studies, but it didn’t seem to help. Evidence does NOT support.

60
Q

Nitric oxide in ARDS: yes or no

A

It does seem to transiently improve oxygenation, but doesn’t increase survival or decrease ventilation time, so there’s kinda no point.

(HGC) ACNP804 Exam 4 (8 decks)

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