Lec 14 ARDS Flashcards

1
Q

What characterizes ARDS?

A
  • PaO2/FiO2 < 200
  • hypoxemia
  • bilateral lung infiltrates
  • no left atrial HTN
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2
Q

What characterizes acute lung injury [ALI]?

A

Pao2/FIO@ < 300

less severe hypoxemia

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3
Q

What is most important cause of ARDS?

A

sepsis

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4
Q

What are some things that cause ARDS?

A
sepsis
pneumonia
aspiration
pancreatitis
trauma
burn
trasnfusion
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5
Q

What is incidence of acute lung injury? ARDS?

A

acute lung injury = 80 / 10,000

ARDS = 59 / 10,000

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6
Q

What do you see on pathology in ARDS?

A

diffuse alveolar damage [DAD}
failure of alveolar capillary membrane and flooding of alveolar airspaces with proteinaceous fluid

oxygen derived free radicals cause microvascular injury and multi-organ failure

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7
Q

What inflammatory cytokines involved in development of ARDS?

A

TNF-alpha
IL-1
IL-8

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8
Q

What happens to surfactant in ARDS?

A

have depletion of surfactant –> atelectasis, gas exchange disturbance and decreased pulmonary compliance

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9
Q

What happens to microcirculation in ARDS?

A

altered NO and cytokine induced activation of coagulation cascade

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10
Q

What happens to fibroblasts in late phase ARDS?

A

fibroblasts proliferate

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11
Q

What is VILI?

A

ventilator induced lung injury = caused by us; we give positive airways pressure ventilation

since ARDS is patchy –> there are patches of normal lung that get injured by the ventilation

cause barotrauma and volutrauma –> cytokines released

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12
Q

What is history of ARDS?

A

edema phase = 1st 2 days –> alveolar capillary basement membrane broken down; proteinacious fluid exudes into alveolar space

hyaline membranes organizing = starts day 2; peaks day 4 and declines by day 7

fibroblast proliferation = starts day 7 –> leads to interstitial fibrosis

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13
Q

What is exudative vs proliferative phase of ARDS?

A

exudative = 1st week; have edema + hyaline membranes

proliferative = 2nd week; have interstitial inflammation + fibrosis due to fibroblast proliferation

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14
Q

What is triad for ARDS diagnosis?

A

bilateral lung infiltration
hypoxemia
no LA hypertension

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15
Q

What does imaging tell you in ARDS?

A
  • necessary for diagnosis to see bilateral lung infiltrate

- tells you nothing about the stage

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16
Q

What is treatment for ARDS?

A

treat underlying cause [sepsis, pneumonia, etc]

due low tidal volume ventilation to avoid VILI

17
Q

What is the only ARDS treatment with known mortality benefit?

A

low tidal volume ventilation

18
Q

What is mortality of ARDS?

A

28-42%

19
Q

How does ARDS mortality differ with diagnosis?

A

worse prognosis if sepsis related compared to trauma/transfusion related

20
Q

What are predictors of ARDS mortality?

A
  • advanced age
  • sepsis
  • degree of other organ dysfunction
  • co-morbidities
21
Q

What happens to lung function after ARDS?

A
  • survivors can have persistent restrictive impaired lung function
22
Q

What are some non=pulmonary sequelae in ARDS?

A
  • muscle wasting
  • polyneuropathy
  • neurocognitive impairment
  • depression
  • anxiety
  • PTSD
23
Q

What happens in neonatal respiratory distress syndrome?

A
  • happens in premature babies < 37 wks
  • have lack of surfactant –> rapid shallow breathing, flaring, retraction, cyanosis within minutes of birth
  • ground glass on chest xray
24
Q

What are findings in neonatal RDS?

A
  • hypoxemia, hypercapnea

- ground glass on chest xray

25
Q

Who is most at risk for neonatal RDS?

A
  • premature babies

- mother with diabetes

26
Q

How do you prevent neonatal RDS?

A

steroids to induce surfactant production between 24-34 wks of pregnany

27
Q

What is treatment for neonatal RDS?

A
  • CPAP
  • vent support
  • minimize O2 tox
  • artificial surfactant
28
Q

What is clinical course of neonatal RDS?

A

worse over 2-4 days then improved