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Pulmonology > Lecture 14: Pulmonary Edema and ARDS > Flashcards

Lecture 14: Pulmonary Edema and ARDS Flashcards

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1
Q

Starling equation

A

F = K [(Pc – Pis) – sigma(COPc-COPis)]

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2
Q

Pulmonary capillary pressure is higher/lower than peripheral capillary pressure

A

Lower (~10 mm Hg)

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3
Q

Net hydrostatic pressure in lungs favors…

A

Fluid extrusion (15 mm Hg OUT)

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4
Q

Osmotic pressure in lungs favors…

A

Fluid in (14 mm Hg)

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5
Q

Net Starling forces in lungs slightly favor…What happens under normal circumstances?

A

Loss of fluid (filtration out of pulmonary capillaries); lymphatic vessels drain interstitial space

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6
Q

Does fluid filtered from circulation normally enter the alveoli?

A

No, typically have very tight junctions → only if sufficient fluid builds up to damage alveolar epithelium

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7
Q

What variable in Starling’s equation is altered in cardiac failure?

A

Increased Pc → “hydrostatic” pulmonary edema

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8
Q

In what setting would we have increased “k”?

A

Breakdown of barriers → increased permeability

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9
Q

What are two lymph-related reasons for pulmonary edema? How is the lymph protective?

A

Increased central venous pressure/obstruction of lymphatics; lymph reserve = 10-fold increase in lymph system before lung water increases

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10
Q

What can cause decreased COPc? Does this cause pulmonary edema? Why or why not?

A

Hypoalbuminemia; nope → fall in COPc is associated with parallel decline in COPis

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11
Q

Define Acute Respiratory Distress Syndrome (ARDS) (4 components)

A

Increased permeability (non-cardiogenic) pulmonary edema, lung inflammation, hypoxemia, and decreased compliance

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12
Q

Criteria for ARDS (4)

A
  1. Timing (w/in a week of precipitating event); 2. Chest imaging (bilateral opacities); 3. Hypoxemia (PaO2/FiO2 ratio less than 300 mm Hg); 4. Origin of edema (non-cardiogenic)
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13
Q

ARDS etiology: direct injury

A

Pneumonia, aspiration, contusion, hyperoxia (can cause alveolar injury), toxic inhalation, near-drowning

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14
Q

ARDS: indirect injury. Which is the most common?

A

Sepsis (most common), major trauma (fat embolism from broken bone), multiple bone transfusions, pancreatitis (enzymes released in circulation), cardiopulmonary bypass, drug overdose, medications, urema

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15
Q

ARDS pathogenesis

A

Injury to pneumocytes → pro-inflammatory cytokines → neutrophils and their products → tissue damage/increased permeability → protein escape from vasculature → air spaces fill with proteinaceous edema AND loss of surfactant → alveolar collapse

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16
Q

Stages of ARDS pathology (3)

A

Exudative (up to 7 days; edema, hyaline membranes) → proliferative (2 weeks; proliferation of cells, inflammation) → fibrotic (3 weeks)

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17
Q

What is and where is the edema in exudative stage

A

Protein/neutrophil-rich in alveolar spaces

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18
Q

What is the “hyaline membrane”

A

Protein-rich edema fluid that has filled alveoli and lines alveolar membrane

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19
Q

Describe the proliferative stage

A

Some edema/infiltrates absorbed, type II cells replicate to replace damaged type I cells, hyaline membrane reorganized, obliteration of pulmonary vessels, accumulation of fibroblasts in pulmonary parenchyma

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20
Q

Describe fibrotic stage. Does this always happen?

A

Lung parenchyma not repaired, but develops fibrosis scarring; not everyone progresses to this stage

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21
Q

What channels are involved in removal of pulmonary edema?

A

Na+/Cl- via apical alveolar epithelial channels and Na/K ATPase on basolateral side; water transport is passive

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22
Q

Which type of pulmonary edema resolves faster?

A

Cardiogenic, because the tissue itself isn’t as damaged

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23
Q

How do the proteins get out in ARDS?

A

Paracellular diffusion and endocytosis via epithelial cells/macrophages

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24
Q

ARDS pathophysiology

A

V/Q mismatch due to decreased V (shunt) → hypoxemia; alveolar collapse/atelectasis; increased pulmonary vascular resistance due to hypoxic vasoconstriction → pulmonary hypertension

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25
Is hypercapnia common in ARDS?
No due to increased ventilation in unaffected alveoli
26
Why does pulmonary hypertension occur?
Fluid in interstitium increases interstitial pressure, compressing bronchus (wheezing) and artery (hypertension)
27
What can pulmonary hypertension lead to?
RV heart failure
28
Describe the relationship between lung compliance (why?) and ARDS. What about hysteresis?
Decreased lung compliance; why? SOME alveoli not functioning SO less volume enters lung during inflation (definition of compliance); hysteresis is increased because higher pressures are required to OPEN collapsed airways
29
FRC and ARDS. Clinical manifestation?
Decreased; rapid and shallow (causes dyspnea)
30
ARDS radiology findings
Bilateral opacities with “ground glass” appearance; some areas of lung that are normal and some that are collapsed (based on gravity)
31
ARDS clinical presentation
Features w/ in 6 to 72 hours of inciting events; symptoms: dyspnea, cough/chest pain; tachypnea, cyanosis, rales
32
How do we grade ARDS severity?
PaO2 to PiO2 ratio: mild
33
ARDS treatment. What are you trying to prevent?
Treat precipitating disorder and support gas exchange (mechanical ventiliation); patients tend to die of sepsis and multiorgan failure
34
Describe “positive pressure” breathing
Occurs when Palv becomes more positive with inspiration → at the end of inspiration, Palv will be positive (as opposed to zero)
35
Define Positive End-Expiratory Pressure (PEEP)
Maintains positive pressure in airway at the end of expiration to prevent collapse of alveoli (pressure is always above “closing pressure”)
36
How can a ventilator cause harm?
Volutrauma, barotraumas, atelectrauma
37
Describe volutruma and prevention
Over distention of lung units → alveolar strain due to high tidal volumes which can worsen ARDS; prevent w/ low tidal volume ventilation and increased RR
38
What is an effect of low tidal ventilation?
Increased PACO2
39
Describe barotrauma and prevention
Excessive airway pressure can lead to pneumothorax and air in other places; prevent w/ low pressure
40
Describe alectrauma and prevention
Repetitive opening and closing of terminal lung units associated with mechanical ventilation can be detrimental; prevent w/ PEEP
41
Cause of neonatal respiratory distress syndrome. What trimester do you get surfactant?
Deficiency of surfactant → alveolar collapse; 3rd trimester
42
RDS prevention and treatment (2)
Antenetal corticosteroids to pregnant women at 23-34 weeks at risk of preterm birth to induce enzymes that stimulate release of surfactant; tx = positive pressure ventilation and exogenous surfactant administration
43
Major categories of interstitial lung disease (4)
Fibrosing/inflammation, granulomatus, smoking-related, other
44
Most common histological finding of ARDS. What is if this finding called if it’s idiopathic?
Diffuse alveolar damage (DAD) = acute interstitial pneumonia (AIP)/Hamman-Rich syndrome
45
Two less common findings of ARDS
Diffuse alveolar hemorrhage, eosinophilic pneumonia
46
Cryptogenic organizing pneumonia typically presents more…
Subacute
47
DAD: what it is, how serious, problem with treatment, radiology
Diffuse alveolar capillary and epithelial damage related to single insult and rapid onset of severe, life-threatening respiratory insufficiency that is often refractory to O2 therapy, radiological finding is diffuse alveolar infiltration
48
What can cause ARDS, broadly? (5)
Infection, injury, irritants, uremia, pancreatitis
49
Pathogenesis of DAD
Injury to vascular endothelium and alveolar epithelium → proteinaceous fluid leak into alveoli with type II cell proliferation → fibrosis
50
Important pathological hallmark of DAD
Hyaline membranes, which are replaced during proliferative phase
51
Phases and days of DAD
Exudative (1-7); Proliferative (7-21); Fibrotic (>21)
52
Gross features of DAD (4)
Wet, boggy, airless, heavy
53
Describe histology of exudative phase
Eosinophilic structures lining alveolar spaces (hyaline membrane) w/ interstitial and alveolar edema
54
Describe histology of organizing phase
Hyaline membrane is organizing, fibroblastic proliferation within interstitium, type II pneumocyte hyperplasia
55
Pathological subtypes of eosinophilic pneumonia
1. Simple, 2. Tropical, 3. Chronic, 4. Acute
56
Describe simple eosinophilic pneumonia
Fleeting pulmonary infiltrates and peripheral blood eosinophilia
57
Describe tropical eosinophilic pneumonia
High fever, wheezing, peripheral blood eosinophila often due to parasitic infection
58
Describe chronic eosinophilic pneumonia
Subacute illness with fever, dyspnea, peripheral blood eosinophilia often w/ asthma history; patchy infiltrates that will resolve and reappear; often idiopathic or due to some sort of toxicity
59
Describe acute eosinophilic pneumonia. Histology?
Acute onset respiratory failure (ARDS) but absent peripheral blood eosinophila; hyaline membranes with eosinophils WITHIN
60
Histological findings of eosinophilic pneumonia
Intra-alveolar fibrin, macrophages, abundant eosinophils
61
Eosinophilic pneumonia is sensitive to…
Steroids
62
Describe organizing pneumonia and three settings
Airspace organization = loose CT in alveoli as the lung attempts to repair seen as a primary process, a component of another process (acute pneumonia), or a secondary reaction to something unrelated (next to a lesion/tumor)
63
Describe organizing pneumonia pattern and histological findings
Specific pattern of OP around small airways associated with subacute cough and SOB; histologically it looks like ORGANIZING FIBROBLASTIC TISSUE within airspaces with little interstitial involvement and normal intervening lung
64
What is the idiopathic name of organizing pneumonia pattern?
Cryotogenic organizing pneumonia (COP)
65
What are some causes of organizing pneumonia pattern?
Collagen/vascular disease, drug reaction, etc.

Pulmonology (21 decks)

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