ARDS Flashcards

1
Q

Three characteristics of pulmonary edema:

A
  1. Heavy, wet lungs: basal initiation (dependent edema)
  2. Hemodynamic: Cardiogenic
  3. Permeability: increased capillary permeability
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2
Q

Pulmonary edema: hemodynamic characteristics

A
  1. Increased hydrostatic pressure: left sided CHF
  2. Engorged alveolar capillaries
  3. Intra-alveolar granular pink precipitate
  4. Alveolar microhemorrhages
  5. Hemosiderin-laden mac’s (heart cells)
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3
Q

What are the consequences of long-standing pulmonary edema?

A
  1. Mitral stenosis
  2. Increased heart cells
  3. Fibrosis and thickening of alveolar walls
  4. Soggy lungs become brown and indurated (firm or hard due to fibrous elements)
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4
Q

What are the characteristics of microvascular injury in pulmonary edema?

A
  1. Injury to capillaries of the alveolar septa
  2. Primary injury to the vascular endothelium or alveolar epithelial cells: no increase of hydrostatic pressure.
  3. Fluid and proteins into interstitial space and potentially alveoli
  4. Pneumonia=localized edema
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5
Q

Diffuse alveolar damage (DAD) morphology: acute

A
  1. Congestion, interstitial, and intra-alveolar edema, inflammation and fibrin deposition.
  2. Fibrin rich edematous fluid with cytoplasmic and lipid remnants, necrotic epithelial cells.
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6
Q

DAD morphology: organizing type

A
  1. Type II pneumocytes (**) undergo proliferation
  2. Results in organizing fibrin exudate and intra-alveolar fibrosis
  3. Leads to more pneumocyte proliferation and collagen deposition.
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7
Q

ARDS onset:

A
Rapid
Respiratory insufficiency
Cyanosis
Arterial hypoxemia (refractory oxygen therapy)
Multi-organ failure
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8
Q

Chest radiographs of ARDS reveal what?

A

Diffuse alveolar infiltrates

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9
Q

ARDS causes: infectious

A
Sepsis
Viral
Mycoplasma
Pneumocystis 
Miliary TB
Gastric aspiration
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10
Q

ARDS causes: physical

A

Mechanical trauma/head injuries

Burns and radiation

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11
Q

ARDS causes: inhaled irritants

A

Smoke
Gases
Chemicals

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12
Q

ARDS causes: chemical

A

Heroin
Aspirin (ASA)
Barbituates

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13
Q

ARDS causes: hematologic

A

TACO

DIC

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14
Q

Other causes of ARDS:

A

Pancreatitis
Uremia
Bypass Sgx

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15
Q

What happens in ARDS?

A
  1. Capillary endothelial or alveolar epithelial injury.
  2. Increased vascular permeability and flooding.
  3. Decreased diffusion capacity.
  4. Surfactant abnormalities (damaged Type II pneumos)
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16
Q

ARDS in the long run, what happens?

A

Exudate and destruction are poorly resolved.

Leads to organization and scarring-chronic disease

17
Q

Immune responses due to ARDS:

A
  1. Elevated pro-inflammatory mediators.
  2. Decreased anti-inflammatory molecules.
  3. Proinflammatory: NF-kB (required)
  4. Bacterial infection: toll-like receptors–> innate immune response–> NF-kB
    * Effects transcriptional selectivity (increased IL-10)
18
Q

Immediate immunologic reaction to ARDS: what is released?

A

IL-8:

  • neutrophilic chemotactic and activating agent
  • Pulmonary macrophages
19
Q

Released IL-1 and TNF role in ARDS?

A

Further activation and sequestration of neutrophils.

Vascular spaces, intersititium, and alveoli

20
Q

Other things released by ARDS?

A

Oxidants
Proteases
Platelet-activating factor
Leukotrienes

21
Q

ARDS presentations clinically:

A
  1. Radriographs normal at first
  2. Non-homogenous spread.
  3. Decreased functional lung volume.
  4. VQ mismatch
  5. 60% mortality
22
Q

Acute interstitial pneumonia

A
  1. Widespread acute lung injury
  2. Unknown cause
  3. 50 years of age without sex predilection.
  4. Presents like URTI
  5. Progresses similar to ARDS
  6. 50% mortality