ICL 2.0: Acute Respiratory Distress Syndrome

Question 1

what is acute respiratory distress syndrome?

Answer 1

ARDS is a severe inflammatory condition of the lungs that leads to rapid and severe pulmonary injury

it is initially due to damage of the endothelial cells, which line the blood vessels in the lungs –> this damage causes the endothelial cells to become markedly permeable, which leads to leakage of fluid into the supporting tissues of the lungs and the alveoli

this results in lung damage and respiratory failure and poor gas exchange = hypoxemia

Question 2

what do you see histologically with ARDS?

Answer 2

leakage of fluid leads to the formation of intra‐alveolar hyaline membranes (made of proteins and dead cells), which impair gas exchange within the alveolar‐capillary unit

1. thickened inter-alveolar membranes
2. hyaline membranes representing diffuse alveolar damage
3. lots of inflammatory cells

Question 3

what type of pulmonary edema is associated with ARDS?

Answer 3

non-cariogenic edema

this means it’s not due to cardiac dysfunction, but rather to some other insult so these patients have a normal pulmonary capillary wedge pressure (PCWP), which approximates the pressure in the left atrium

Question 4

what is cardiogenic pulmonary edema?

Answer 4

when pulmonary edema has a cardiogenic cause, such as congestive heart failure

you will see an increased pulmonary capillary wedge pressure which approximates the pressure in the left atrium

this occurs because of blood backup in the left side of the heart due to decreased cardiac contractility

Question 5

what are the 4 criteria needed to define ARDS?

Answer 5

1. acute

onset of symptoms must be within 1 week of a known clinical insult or the development of new or worsening respiratory symptoms

2. chest imaging

bilateral opacifications are seen that are not fully explained by effusions, lobar or lung collapse, heart failure or nodules

3. noncardiogenic pulmonary edema

respiratory failure and pulmonary edema are seen that are not fully explained by cardiac failure or fluid overload

4. oxygenation

the ratio of partial pressure of arterial oxygen and fraction of inspired oxygen (PaO2/FiO2) is ≤300 which means poor oxygenation from hyalinization of alveoli and V/Q mismatch

Question 6

what is the PaO2/FiO2 ratio in a person with ARDS?

Answer 6

PaO2/FiO2 < 300 mL

if you give a healthy person 100% FiO2 oxygen and then take a PaO2 will be 600-700 mmHg on the ABG

so if PaO2/FiO2 is less than 300 that means there’s over 1/2 compromise of oxygen exchange and oxygen isn’t diffusing due to the hyalinization from the ARDS

Question 7

what is the pathogenesis of ARDS?

Answer 7

the hallmark of ARDS is diffuse endothelial damage if the pulmonary capillaries caused by some type of physiologic insult

the massive amounts of proinflammatory cytokines present during a septic episode are thought to lead to increased vascular permeability and production of free radicals and other dangerous substrates that harm the pulmonary endothelium

diffuse damage to gas-exchanging surface on either the alveolar or capillary side of the membrane results in increased vascular permeability which causes hylaization and flooding of the alveolar space which consequently leads to pulmonary edema

there’s also loss of surfactant so the alveoli will collapse!

Question 8

what are some of the most common etiologies of ARDS?

Answer 8

1. sepsis
2. pancreatitis
3. pneumonia
4. aspiration
5. uremia
6. trauma
7. shock

septic shock is the most common cause of ARDS

Question 9

how does pancreatitis cause ARDS?

Answer 9

activated, highly potent pancreatic enzymes enter the systemic circulation and lead to endothelial damage in the pulmonary capillaries

Question 10

what are the effects of ARDS on the lungs?

Answer 10

1. capillary leak
2. hyalin membranes
3. surfactant depletion
4. alveolar collapse/consolidation
5. V/Q mismatch and diffusion problems
6. reduced compliance
7. neutrophil infiltration and cytokine release

Question 11

what position do you want the patient to be laying in if they have ARDS?

Answer 11

prone!

it decreases atelectasis and mortality in ARDS patients

Question 12

what is the most common cause of ARDS?

Answer 12

septic shock

Question 13

what is the clinical presentation of ARDS?

Answer 13

1. present with a few hours to day s of the inciting event (it’s a secondary illness)
2. very ill and decompensated quickly
3. dyspnea, SOB, tachypnea
4. hypoxic
5. diffuse crackles on lung exam from hyaline membranes in the alveoli trying to open up
6. respiratory acidosis with hypercarbia and an increased A-a oxygen gradient

Question 14

why do patients with ARDS have hypercarbia?

Answer 14

hyaline membranes don’t contribute to gas exchange

so there’s increased pathological dead space and the body’s unable to compensate

Question 15

why do patients with ARDS have hypoxemia?

Answer 15

1. diffusion impairment from hyaline membrane

2. V/Q mismatch

Question 16

which ethnicity is more effected by COVID?

Answer 16

there are a disproportionate number of COVID fatalities among african americans (40% of deaths even though they’re only 18% of the popualation)

social scientists have attempted to explain the discrepancy by occupational exposures to the service industries, crowded residential spaces, and a greater incidence of morbidity second to poor healthcare access

the social aspect of this disease should not be trivialized and undoubtedly contributes substantially to mortality

Question 17

what are the 5 causes of hypoxemic respiratory failure?

Answer 17

1. decreased FiO2
2. hypoventilation
3. diffusion limitation
4. V/Q mismatch
5. shunt

Question 18

what is the most consistent finding you would expect to see on arterial blood gases taken from patients with ARDS?

Answer 18

increased A-a oxygen gradient

Question 19

how do you treat ARDS?

Answer 19

1. intubation and ventilator
2. treat underlying cause
3. high PEEP
4. low tidal volume ventilation
5. monitor airway pressures
6. conservative fluid management

careful and precise ventilator management is the cornerstone of treating ARDS

Question 20

what are the 2 major ventilator principles used in ARDS patients?

Answer 20

1. high positive end-expiratory pressure (PEEP)
2. low tidal volume ventilation (LTVV) to prevent lung damage

an elevated PEEP promotes decreased collapse of the alveoli – this is of benefit because in ARDS, fully collapsed alveoli are much harder to inflate and lead to worsening lung compliance and V/Q mismatch compared with alveoli that are partially deflated

the LTVV is used because it prevents barotrauma, which is injury to the lung from excessive ventilator pressures

Question 21

what is baby lung?

Answer 21

they have collapsed lungs so when you give a huge tidal volume through the ventilator you over-inflate the baby lung which causes trauma and the release of MORE cytokines and transfer of more bacteria!!

this is why you use low tidal volumes with the ventilators in patients with ARDS

so smaller tidal volumes have decreased mortality, increased number of ventilator free days and decreased extra pulmonary organ failures despite the patients having worse oxygenation, increased pCO2 and lower pH

Question 22

what is the approximate mortality for patients with ARDS?

Answer 22

40%

it’s even lower if you use proning, antibiotics, lung protective strategies it’s more like 25%

Question 23

which of the following would you expect to see in patients with ARDS?

A. decreased cardiac output

B. decreased stroke volume

C. increased plasma concentration of brain natriuretic peptide

D. increased transcription of genes encoding eNACs

E. normal pulmonary capillary wedge pressure

Answer 23

E. normal pulmonary capillary wedge pressure

this is because it’s non-cardiogenic pulmonary edema

Question 24

which of the following parameters falls within the 2012 Berlin diagnostic criteria forARDS?

A. lobar consolidation seen on a chest x‐ray

B. onset of symptoms occur after 10 days of insult

C. PaO2/FiO2 = 400

D. PaO2/FiO2 = 200

E. pulmonary edema secondary to heart failure

Answer 24

D. PaO2/FiO2 = 200

Question 25

what is the rationale for using low tidal volume ventilation in patients with ARDS?

A. decreases breathing rate

B. decreases heart rate

C. increases activation of the parasympathetic nervous system

D. increases cardiac contractility

E. prevents alveolar barotrauma

Answer 25

E. prevents alveolar barotrauma

Question 26

A male is involved in a motor vehicle collision and is brought to the emergency department intubated. He is resuscitated and admitted to the intensive care unit because of severe brain injury. The following day his chest x-ray reveals bilateral fluffy infiltrates. Which of the following is the earliest finding of acute respiratory distress syndrome within 12 to 24 hours after the onset of the disorder?

A. Fever

B. Hypercapnia

C. Extreme hypoxia

D. Tachypnea

Answer 26

D. Tachypnea

this is probably one of the first signs – this happens because they’re extremely hypoxemic