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Pulmonology > Lecture 14: Pulmonary Edema and ARDS > Flashcards

Lecture 14: Pulmonary Edema and ARDS Flashcards

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
Q

Is hypercapnia common in ARDS?

A

No due to increased ventilation in unaffected alveoli

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26
Q

Why does pulmonary hypertension occur?

A

Fluid in interstitium increases interstitial pressure, compressing bronchus (wheezing) and artery (hypertension)

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27
Q

What can pulmonary hypertension lead to?

A

RV heart failure

28
Q

Describe the relationship between lung compliance (why?) and ARDS. What about hysteresis?

A

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
Q

FRC and ARDS. Clinical manifestation?

A

Decreased; rapid and shallow (causes dyspnea)

30
Q

ARDS radiology findings

A

Bilateral opacities with “ground glass” appearance; some areas of lung that are normal and some that are collapsed (based on gravity)

31
Q

ARDS clinical presentation

A

Features w/ in 6 to 72 hours of inciting events; symptoms: dyspnea, cough/chest pain; tachypnea, cyanosis, rales

32
Q

How do we grade ARDS severity?

A

PaO2 to PiO2 ratio: mild

33
Q

ARDS treatment. What are you trying to prevent?

A

Treat precipitating disorder and support gas exchange (mechanical ventiliation); patients tend to die of sepsis and multiorgan failure

34
Q

Describe “positive pressure” breathing

A

Occurs when Palv becomes more positive with inspiration → at the end of inspiration, Palv will be positive (as opposed to zero)

35
Q

Define Positive End-Expiratory Pressure (PEEP)

A

Maintains positive pressure in airway at the end of expiration to prevent collapse of alveoli (pressure is always above “closing pressure”)

36
Q

How can a ventilator cause harm?

A

Volutrauma, barotraumas, atelectrauma

37
Q

Describe volutruma and prevention

A

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
Q

What is an effect of low tidal ventilation?

A

Increased PACO2

39
Q

Describe barotrauma and prevention

A

Excessive airway pressure can lead to pneumothorax and air in other places; prevent w/ low pressure

40
Q

Describe alectrauma and prevention

A

Repetitive opening and closing of terminal lung units associated with mechanical ventilation can be detrimental; prevent w/ PEEP

41
Q

Cause of neonatal respiratory distress syndrome. What trimester do you get surfactant?

A

Deficiency of surfactant → alveolar collapse; 3rd trimester

42
Q

RDS prevention and treatment (2)

A

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
Q

Major categories of interstitial lung disease (4)

A

Fibrosing/inflammation, granulomatus, smoking-related, other

44
Q

Most common histological finding of ARDS. What is if this finding called if it’s idiopathic?

A

Diffuse alveolar damage (DAD) = acute interstitial pneumonia (AIP)/Hamman-Rich syndrome

45
Q

Two less common findings of ARDS

A

Diffuse alveolar hemorrhage, eosinophilic pneumonia

46
Q

Cryptogenic organizing pneumonia typically presents more…

A

Subacute

47
Q

DAD: what it is, how serious, problem with treatment, radiology

A

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
Q

What can cause ARDS, broadly? (5)

A

Infection, injury, irritants, uremia, pancreatitis

49
Q

Pathogenesis of DAD

A

Injury to vascular endothelium and alveolar epithelium → proteinaceous fluid leak into alveoli with type II cell proliferation → fibrosis

50
Q

Important pathological hallmark of DAD

A

Hyaline membranes, which are replaced during proliferative phase

51
Q

Phases and days of DAD

A

Exudative (1-7); Proliferative (7-21); Fibrotic (>21)

52
Q

Gross features of DAD (4)

A

Wet, boggy, airless, heavy

53
Q

Describe histology of exudative phase

A

Eosinophilic structures lining alveolar spaces (hyaline membrane) w/ interstitial and alveolar edema

54
Q

Describe histology of organizing phase

A

Hyaline membrane is organizing, fibroblastic proliferation within interstitium, type II pneumocyte hyperplasia

55
Q

Pathological subtypes of eosinophilic pneumonia

A
  1. Simple, 2. Tropical, 3. Chronic, 4. Acute
56
Q

Describe simple eosinophilic pneumonia

A

Fleeting pulmonary infiltrates and peripheral blood eosinophilia

57
Q

Describe tropical eosinophilic pneumonia

A

High fever, wheezing, peripheral blood eosinophila often due to parasitic infection

58
Q

Describe chronic eosinophilic pneumonia

A

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
Q

Describe acute eosinophilic pneumonia. Histology?

A

Acute onset respiratory failure (ARDS) but absent peripheral blood eosinophila; hyaline membranes with eosinophils WITHIN

60
Q

Histological findings of eosinophilic pneumonia

A

Intra-alveolar fibrin, macrophages, abundant eosinophils

61
Q

Eosinophilic pneumonia is sensitive to…

A

Steroids

62
Q

Describe organizing pneumonia and three settings

A

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
Q

Describe organizing pneumonia pattern and histological findings

A

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
Q

What is the idiopathic name of organizing pneumonia pattern?

A

Cryotogenic organizing pneumonia (COP)

65
Q

What are some causes of organizing pneumonia pattern?

A

Collagen/vascular disease, drug reaction, etc.

Pulmonology (21 decks)

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