Brainscape's Knowledge GenomeTM

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


See full index

Boards: Respiratory > Acute Respiratory Distress Syndrome 2022. Lancet > Flashcards

Acute Respiratory Distress Syndrome 2022. Lancet Flashcards

1
Q

What is the most common cause of ARDS?

A

sepsis, and specifically pneumonia (pulmonary sepsis)

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

List the most common non-infectious causes of ARDS

A
  • pancreatitis
  • aspiration of gastric contents
  • severe traumatic injuries with shock and multiple transfusions

transfusion can also cause ARDS in itself (TRALI)

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

Why do traumatic injuries not cause ARDS as commonly as they used to?

A

changes in mechanical ventilation, crystalloid resuscitation, and transfusion strategies

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

Fill in the blanks for causes of ARDS

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

Where do hyaline membranes form in ARDS lungs?

A

along the damaged alveolar basement membrane

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

Describe the epithelial and endothelilal injuries sustained in mild ARDS seen in this picture

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

Describe the epithelial and endothelial injuries/changes sustained in severe ARDS seen in this picture

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

Describe the process of alveolar flooding in ARDS

A
  • disruption of tight junctions –> fluid leakage into the air space (alveolar flooding) = protein-rich pulmonary edema
  • fluid cannot be removed due to impaired Na transport –> cannot maintain dry airspace

consequences:

  • flooding inactivates surfactant - microatelectasis, end-expiratory alveolar collapse
  • flooding impairs gas exchange - ventilation-perfusion mismatch and shunt
  • decreased lung compliance - requires higher inspiratory pressure and increased work of breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the main components of the glycocalyx?

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

Describe the changes leading to hyaline membrane formation in ARDS

A

activation and injury of the alveolar epithelium –> loss of anticoagulant molecules + release of TF –> favors intraalveolar fibrin formation –> hyaline membrane formation

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

Name examples of adhesion molecules and endothelilal injury mediators that are upregulated in endothelial injury in ARDS

A

adhesion molecules: P-selectin, E-selectin
endothelial injury mediator: angiopoietin-2

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

List examples of stimuli that may trigger endothelial injury in ARDS

A
  • DAMPS
  • PAMPS
  • proinflammatory cytokines
  • cell-free hemoglobin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is epithelial lung injury suspected to lead to endothelial injury in the pulmonary capillaries?

A

cell-to-cell communicaiton and transfer of ROS between the epithelial and endothelial cells

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

What are the consequences of miscovascular thrombosis in ARDS?

A
  • deadspace ventilation
  • pulmonary arterial hypertension - right vetricular dysfunction if severe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain how neutrophils are recruited in ARDS

A

Mostly recruited by macrophages:
* DAMPS and PAMPS bind to macrophage PRR
* activates macrophages to inflammatory phenotype
* release of proinflammatory cytokines and neutrophil chemoattractants (e.g., interleukin-8)

lung epithelial cells also release neutrophil chemoattractants

neutrophils enter lungs through the capillary walls following the chemoattractant gradient - paracellularly between endothelial cells and alveolar epithelial cells

transcytosis possible

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

Explain how neutrophils cause alveolar damage

A
  • release of ROS, proteases, proinflammatory lipid-derived mediators (prostaglandins, leukotrienes)
  • NETs (DNA, histones, proteases) –> increase inflammation by activating NRLP3 inflammasome –> initiates release of IL-1-beta and IL-18
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the main components of neutrophilic extracellular traps

A

DNA
histones
proteases

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

Describe the “baby lung” concept

A

heterogeneity and decreased compliance of diseased lungs leads to small portion of lungs parechyma participating in alveolar ventilation

tidal volumes resembling babies

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

How does repetetive cyclic stretching cause pulmonary injury?

A
  • stretching on cellular level - creates gaps between pulmonary epithelial cells –> disconnect from basememnt membrane, cellular necrosis
  • cyclic stretching initiates inflammatory response –> mechanosensitive proinflammatory pathways –> cytokines and chemokines released
  • stretch-induced cytosolic calcium oscillations –> affects ATP production
  • impairs alveolar epithelial fluid transport
20
Q

Name 2 proresolving mediators facilitating resolution of ARDS

A
  • lipoxins
  • resolvins
21
Q

How are intraalveolar neutrophils removed during the resolution of ARDS?

A

apoptosis –> then removed by alveolar macropahges

22
Q

Name processes needed to resolve pulmonary edema in ARDS

A
  • resolution of hyperpermeability
  • normalization of microvascular pressure
  • restoration of alveolar epithelial fluid transport (i.e., epithelial cells must have functioning Na and Cl transport)
23
Q

Name endogenous factors that can upregulate alveolar fluid clearance

A
  • catecholamines
  • corticosteroids
24
Q

What is prognostic enrichment?

A

selective inclusion of a phenotype of a disease that is more likely to develop the primary outcome assessed in a study

increases statistical power

e.g., assessing heparin versus no heparin administration on the effect of cardiovascular event in sepsis - include sepsis phenotypes that are more likely to have cardiovascular event anyways

25
Q

What is predictive enrichment?

A

selective inclusion of an endotype of a disease to study an intervention that targets that disease

endotype may benefit more from intervention than unselected population

26
Q

What are the different subphenotype cateogories of ARDS?

A
  • subphenotype by cause
  • biological subphenotype
  • radiological subphenotype
  • physiological subphenotype
27
Q

Compare pulmonary and extrapulmonary causes of ARDS in terms of their primary location of injury and distribution

A

pulmonary cause of ARDS - alveolar epithelial injury and alveolar inflammation prioritized - may be more localized and heterogenous

extrapulmonary cause of ARDS - endothelial injury and systemic inflammation prioritized whole lung is affected by endothelial dysfunction - diffuse injury pattern

28
Q

When hyperinflammatory and hypoinflammatory subphenotypes of ARDS were established, how did the cytokines and chemokines compare between the two?

A

hyperinflammatory –> more IL-6, IL-8, and TNF-receptor-1
hypoinflammatory –> more bicarbonate, protein-C

29
Q

What are the two main radiologic phenotypes of ARDS and what are different ventilation strategies to be applied to each?

A

focal subphenotype - respond better to prone positioning

non-focal subphenotype - respond better to alveolar recruitment maneuver

30
Q

What is the key difference between acute hypoxemic respiratory failure and ARDS?

A

ARDS has bilateral infiltrates on chest imaging

31
Q

List the criteria of the Berlin definition of ARDS

A
32
Q

What is the Kigali modification of the ARDS criteria? How does it perform compared to the Berlin criteria?

A

criteria applicable to resource-limited settings:
* removes the requirement of PEEP
* replaces PF ratio with SF ratio
* replaces chest imaging with lung ultrasound

High rate of false positive - i.e., not specific - attributed to the high sensitivity of lung ultrasound

SF ratio with disparities due to skin color differences

33
Q

what are the two main strategies of lung protective ventilation?

A

low tidal volumes - < 6 mL/kg
low plateau pressure - < or equal 30 mm Hg

34
Q

What is airway pressure release ventilation and what is the current evidence for its use in ARDS patients?

A

pressure controlled ventilation which delivers a prolonged high level of pressure with intermittent, time-cycled pressure relase to low level of pressure

meta-analysis –> improved hospital mortality, ventilation-free days, ICU length of stay
BUT methodological limitations

no robust clinical trial proving benefit

35
Q

What category of ARDS patients is high PEEP reserved for?

A

moderate-to-severe ARDS

36
Q

What PEEP and recruitment maneuvre stragies have been shown most beneficial in a recent meta-analysis on ARDS?

A

most beneficial for improving mortality: higher PEEP without recruitment maneuvre

37
Q

What is the recommended upper limit for driving pressures during ventilation in ARDS?

How does driving pressure correlate with mortality?

A

upper limit of 15 cm H2O

38
Q

Define mechanical power in mechanical ventilation

A

the amount of energy transferred from a mechanical ventilator to the respiratory system per unit of time

determined by:
* tidal volume
* driving pressure
* respiratory rate
* inspiratory flow
* PEEP
* mechanical properties of the lung (elastance, airway resistance, etc.)

Unit J/min

39
Q

What is the current recommendation for neuromuscular blockage in ARDS patients?

A

routine use of continuous neuromuscular blockage not recommended, but emphasize there may be a subpopulation of patients with dyssynchrony that could benefit

(ROSE trial)

40
Q

What is the recommendation for ECMO use in ARDS?

A

patients with “severe ARDS” are recommended to be treated with ECMO

41
Q

What are the phases of ARDS? What is their duration?

A

Exudative phase (first 1-7 days)
* initial trigger (endothelial or epithelial primary injury –> DAMPs/PAMPs –> macrophage activation –> inflammatory cytokines attracting neutrophile
* epithelial and endothelial damage –> alveolar fludding
* surfactant dysfunction
* microvascular clots
* etc.

Fibroproliferative phase (weeks following exudative phase, but can start as soon as 48 hours after onset of ARDS)
* type II pneumocyte proliferation
* interstitial fibrosis and exudate organization
* reduced lung compliance

42
Q

What needs to happen for ARDS resolution?

A
  • apoptosis of neutrophils
  • termination of fibroproliferation
  • reabsorption of alveolar edema
  • type II pneumocytes need to differentiate to type I pneumocytes
43
Q

What are the 4 categories of VILI?

A
  • volutrauma
  • barotrauma
  • biotrauma
  • atelectrauma
44
Q

What are reportedly common causes of ARDS in SA?

A
  • Aspiration pneumonia in dogs
  • SIRS and sepsis in dogs and cats
45
Q

List the VetARDS criteria

A
  1. acute onset (<73 hours) tachypnea and breahting difficulties
  2. known risk factor
  3. evidence of pulmonary capillary leak without increased pulmonary capillary pressure (xrays, CT, proteinaceus fluid, extravascular lung water)
  4. Evidence of inefficient gas exchange (low PF, elevated A-a gradient, venous admixture)
  5. optional: evidence of diffuse pulmonary inflammation

Boards: Respiratory (27 decks)

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