03b: ARDS

Question 1

Lung alveoli remain “water-free” via which mechanisms?

Answer 1

1. Tight junctions in endothelial and ESP epithelial cell layers
2. Lymphatic trainage

Question 2

Starling equation depicts net force that drives water from lung (X) into (Y).

Answer 2

X = microvasculature 
Y = interstitial space

Question 3

Pulmonary edema can occur via one of which mechanisms? Star the cause (if any) that preserves lung architecture.

Answer 3

1. Permeability increased (non-cardiogenic)

2. Hydrostatic P increased (cardiogenic)*

Question 4

T/F: It’s possible to tell if pulmonary edema is cardiogenic or non-cardiogenic by CXR.

Answer 4

True - check diaphragmatic angle (spared in non-cardiogenic)

Question 5

Cardiogenic pulmonary edema: a result from (increase/decrease) in P of which heart chamber?

Answer 5

Increase;

LA

Question 6

T/F: ARDS is a syndrome of chronic respiratory failure.

Answer 6

False - acute

Question 7

List some clinical states associated with ARDS.

Answer 7

1. Shock
2. Infection
3. Trauma
4. Liquid aspiration
5. Drugs
6. Inhaled toxins

Question 8

Pathogenesis of ARDS (epithelial injury): proposed pathway initiated by (intra/extra)-cellular (X), produced by (Y).

Answer 8

Extracellular
X = accumulation of oxidants
Y = cell surface NADPH oxidase complex in alveolar macrophages (in response to injury)

Question 9

Pathogenesis of ARDS (epithelial injury): (extra/intra)-cellularly accumulated (X) target (Y), which act as endogenous ligands to (activate/suppress) (Z).

Answer 9

Extracellularly;
X = oxidants
Y = unsaturated phospholipids in surfactant
Activate
Z = TLR4 signaling on macrophage

Question 10

Pathogenesis of ARDS (epithelial injury): Macrophage (X) signaling pathway is activated and induces which cytokine?

Answer 10

X = TLR4

IL-6 (amplifies acute inflammatory response)

Question 11

T/F: Both severity and progression of ARDS are determined by magnitude of oxidative stress AND response of innate immune system.

Answer 11

True

Question 12

T/F: Leukocytes were studied as mediators of final common pathway for ARDS, so severe ARDS unlikely to occur in neutropenic patients.

Answer 12

False - severe ARDS can still occur in the absence of leukocytes

Question 13

T/F: Bottom line/end result of ARDS is overwhelming interstitial fibrosis and collagen deposition.

Answer 13

False - extensive damage to gas-exchanging surface

Question 14

“Berlin” definition of ARDS looks at which 4 characteristics?

Answer 14

1. Timing (insult in past week or new/worsening resp symtpoms)
2. Imaging (bilateral opacities)
3. Edema (not due to HF/volume overload)
4. Oxygenation (PaO2/FiO2 ratio)

Question 15

“Berlin” definition of ARDS: Mild, moderate, severe categories are established based on (X).

Answer 15

X = oxygenation (PaO2/FiO2 ratio)

Mild: 300-200
Mod: 200-100
Severe: under 100

Question 16

Main goal of ARDS therapy:

Answer 16

Maintain gas exchange and hemodynamics until lung can repair itself (no drugs known to accelerate this recovery)

Question 17

T/F: All supportive measures used in ARDS has potential to cause further injury.

Answer 17

True

Question 18

In ARDS therapy, it’s crucial to assist (X) by mechanical ventilation and (Y).

Answer 18

X = work of breathing
Y = PEEP (Positive End Expiratory Pressure)

Question 19

How does PEEP work to assist (X) in ARDS?

Answer 19

X = work of breathing

Increases FRC (which increases compliance and opens/recruits collapsed lung units)

Question 20

ARDS: Mechanical ventilation can involve “lung protective” strategy if (volume/pressure) cycled ventilator is used with (high/low) (X) volume.

Answer 20

Volume;

Low TV

Question 21

Supplemental O2 alone (capable/incapalbe) of raising PaO2 in ARDS. Why?

Answer 21

Incapable;

Resistant hypoxemia is result of intra-alveolar shunting

Question 22

T/F: PEEP in ARDS therapy is converting intra-alveolar shunt to V/Q mismatch.

Answer 22

True (one that responds to O2 therapy)

Question 23

T/F: Trial found that lower (5 cm H2O) PEEP had better outcomes than higher (10 cm H2O) PEEP.

Answer 23

False - no difference in outcome;

So use less! Minimizes further risks of injury

Question 24

ARDS maintenance/therapy: important to maintain oxygen delivery to tissues by measuring/monitoring which factors?

Answer 24

1. CO (via urine output, mental status)
2. Hgb (over 7 g/dL blood)
3. SaO2 (over 90%)

Question 25

ARDS maintenance/therapy: metabolic abnormalities should be corrected. This involves daily monitoring of…

Answer 25

1. Electrolytes
2. BUN, Creatinine
3. Coagulation
4. Glucose/nutrition

Question 26

T/F: In ARDS, avoiding/treating infections includes prophylaxis.

Answer 26

False

Question 27

Sepsis before ARDS likely originated from (X). Sepsis after ARDS likely originated from (Y).

Answer 27

X = abdomen
Y = lungs (pneumonia)

Question 28

T/F: Little evidence exists to support use of steroids in ARDS.

Answer 28

True - bad news outweigh good news

Question 29

Using the Berlin Definition of ARDS, mortality is related to (X). How high is this mortality in mild/mod/severe ARDS?

Answer 29

X = severity of gas-exchange abnormality

20%, 41%, 52% respectively

Question 30

T/F: Implementation of “lung protective strategy” for mechanical ventilation will not reduce overall mortality in severe ARDS.

Answer 30

False - reduces it, but mortality is still mainly related to severity of disease

Question 31

T/F: Using Swan-Ganz catheter to assess volume status in ARDS patient will increase his/her risk for mortality.

Answer 31

True

Question 32

Early death from ARDS is due to (X). Late death is due to (Y). Star the more common scenario.

Answer 32

X = Resp failure (catastrophic lung injury)
Y = Sepsis/SIRS or MSOF (multi-system organ failure)***

Question 33

T/F: Latest findings indicate that ARDS survivors have high prevalence of non-respiratory morbidity.

Answer 33

True

Question 34

A history of (X) has been shown to increase incidence and mortality in ARDS.

Answer 34

X = alcoholism

Due to Cys, and thus glutathione (essential antioxidant), deficiency