ARDS

Question 1

ARDS diagnostic criteria must include what 5 things?

Answer 1

• Presentation within one week of known clinical insult
• Origin of pulmonary edema is non-cardiogenic
• CXR shows bilateral opacities not fully explained by pleural effusion
• Acute hypoxemic RF (mild, mod, severe based on PaO2:FiO2 ratio)
• Decreased lung compliance

Question 2

Provide a few examples of direct insults that result in ARDS?

Answer 2

Pneumonia, aspiration, pulmonary contusion, near drowning, toxic inhalation, oxygen toxicity

Question 3

Provide a few examples of indirect insults that result in ARDS?

Answer 3

Sepsis, severe pancreatitis, shock states, non-thoracic trauma, hypertransfusion, DIC

Question 4

Describe the three pathophysiological changes that occur in ARDS?

Answer 4

1. Alveolar epithelial changes
2. Endothelial changes
3. Compression of small airways

Question 5

What is the pathophysiology that occurs during the alveolar epithelial changes during ARDS (type 1 cell damage)? What manifestations might we see?

Answer 5

Shift in fluids result in type 1 cell damage. This results in decreased SA, increased AC membrane thickness, and decreased diffusion. All result in impaired gas exchange. SOB, increased RR, coarse crackles (fluid shift), decrease O2 sat, decreased PaO2, decrease a/e, bronchial breath sounds all over.

Question 6

What is the patho that occurs during the compression of small airways during ARDS?

Answer 6

Airway resistance increases, WOB increases, alveolar hypoventilation occurs and a V/Q mismatch ensues

Question 7

What is the patho that occurs during the endothelial changes of ARDS (type 2 cell damage)? What manifestations might we see?

Answer 7

Increased cap permeability, micro emboli formation and pulmonary vasoconstriction all occur. Micro emboli and pulmonary vasoconstriction result in regionally altered BF which increase PVR, this leads to alveolar dead space, V/Q mismatch and impaired gas exchange and refractory hypoxemia. Increased ETCO2, increased PaCO2, SOB, SOB, crackles, increased PIP/plat pressure, decreased Vt, pneumothorax, increased WOB, pleural effusion.

Question 8

What is the patho that occurs in airway changes of ARDS? What manifestations might we see?

Answer 8

Fluid shifts result in compression of small airways, increased airway resistance, inc WOB, decreased ventilation. Increased PIP, increased RR, wheeze, increased secretions.

Question 9

What is the patho that occurs in endothelial changes of ARDS? What manifestations might we see?

Answer 9

Microemboli formation (coagulation cascade), increased capillary permeability and pulmonary vasoconstriction result in regionally altered BF resulting in a V/Q mismatch (deadspace-like). Will see decreased preload from increased capillary permeability and fluid shifts, crackles, pulmonary edema, decreased CVP, other signs of decreased preload. Increased PVR, increased PAP, HTN on 2D echo, larger difference between PADP and PCWP (greater than 4 mmHg)

Question 10

What does PaO2:FiO2 ratio >300 signify? What about 200-300? What about 100-200? What about <100?

Answer 10

> 300: normal lung function
200-300: mild ARDS
100-200: mod ARDS
<100: severe ARDS

Question 11

What might we see on the ABGs of someone with ARDS initially? Then what will they progress to? What will the ABG eventually look like?

Answer 11

Resp alkalosis (hyperventilation), respiratory acidosis and then mixed acidosis

Question 12

If a patient has a PA catheter in situ, what is something that would tell us the patient is experiencing significant pulmonary changes?

Answer 12

Difference between PADP and PCWP is greater than 4 mmHG

Question 13

What is the normal difference between PADP and PCWP? What can never happen with these two values?

Answer 13

1-4 mmHg, the PCWP can never be higher than PADP

Question 14

What are four protective lung strategies for ARDS management?

Answer 14

Tidal volumes <6 cc/kg, plateau pressures <30, permissive hypercapnia, and use of PCV to avoid volutrauma

Question 15

What is PIP and plateau pressure significant of?

Answer 15

PIP = dynamic lung compliance

Plat pressure = static lung compliance

Question 16

Why is PIP indicative of dynamic lung compliance?

Answer 16

Influenced by rate of flow of air through airway, the diameter of the airway and lung compliance (airway resistance + lung compliance)

Question 17

Why is plat pressure indicative of static lung compliance?

Answer 17

Measured at end of inspiration, there is no air movement, therefore it is only influenced by lung compliance

Question 18

What is regional over-distention? How does this work?

Answer 18

some alveoli are over-inflated due to the presence of fluid in the lungs - air moves to space with least resistance (no fluid) causing clear alveoli to over-distend

Question 19

What can regional over-distention lead to?

Answer 19

alveolar wall trauma and cell injury causing a release of chemical mediators and a SIRS response in the lungs is perpetuated (further tissue damage, inc cap perm, fluid shifts resulting in worsening pulm edema)

Question 20

What is permissive hypercapnia? How does this benefit someone with ARDS?

Answer 20

Allowing PaCO2 to rise as high as 80-100 mmHg, it is preferred to not let the pH drop less than 7.2. Restricting Vt will increase PaCO2 preventing volutrauma. We can’t compensate by increasing RR as it will decrease our respiratory cycle and increase our flow rate which will increase airway and alveolar pressure

Question 21

When does permissive hypercapnia need to be considered when looking at patient data?

Answer 21

Apply this theory on ABGs when analyzing

Question 22

When would PCV be used in a patient with ARDS? What is the benefit of using PCV?

Answer 22

In the presence of poor lung compliance and increasing plat pressure. Offers slower rate which is more likely to recruit alveoli due to laminar airflow promoting even distribution of air. It decreases airway pressure and opens smaller collapsed airways and improves V/Q mismatching. Also prevents volutrauma. You can set max pressure with each breath.

Question 23

Why is PEEP a mainstay treatment in achieving lower FiO2 levels in those with ARDS? What are some PEEP levels commonly seen in ARDS?

Answer 23

• minimize alveolar collapse
• improve diffusion
• thin AC membrane
• keep air in alveoli at end expiration which lengthens time for gas exchange
  15-18

Question 24

Why is it important to keep FiO2 levels as low as possible in ARDS patients?

Answer 24

minimize risk of alveolar damage from oxygen toxicity (which would precipitate SIRS response in the lungs)

Question 25

What is something we would need to be cautious about when using PEEP in ARDS?

Answer 25

Alveolar damage from inflation of alveoli at end-expiration

Question 26

What is the biphasic fluid replacement strategy for ARDS?

Answer 26

Initially replace with enough fluid to provide hemodynamic restoration, achieve an adequate preload to support optimal CO and O2 delivery
Later: restrict fluids to avoid excessive fluid

Question 27

What is the benefit of using kinetic beds in ARDS?

Answer 27

Dependent lung is always changing which will support V/Q mismatching by perfusing areas with the most ventilation

Question 28

Why is proning a patient helpful in ARDS? How long is someone proned for often?

Answer 28

Perfuses areas of lungs less filled with fluid and consolidation which improves V/Q mismatch. 12-16 hours

Question 29

How does nitric oxide benefit someone with ARDS? What do we see as a result of the administration of this?

Answer 29

Acts on endothelium in lungs and promotes vasodilation to ventilated areas. Decreased PVR, increased BF to ventilated area, decreased V/Q mismatch and improved gas exchange.

Question 30

What are things we can avoid if we use INO? What do we need to be cautious about?

Answer 30

Avoid higher FIO2 levels. Need to be cautious because INO binds with hgb = methhemoglobin which has a higher affinity for O2 (will not give up as easily at the tissue). It is also associated with increased incidence of renal dysfunction.

Question 31

If a patient with ARDS requires fluids how would we want to administer?

Answer 31

Slowly and watch carefully (want to avoid further pulmonary edema)