pulmonary surfactant Flashcards

1
Q

what is surfactant?

A

a surface- active lipoprotein complex formed by the type !! alveolar cells

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2
Q

where is surfactant located?

A

lines the alveoli and the smallest bronchioles

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3
Q

How is surfactant produced?

A

production begins in the type 2 alveolar cells during the terminal stage of lung development (`17-26 wks); lamellar bodies appear in the cytoplasm ~20 wk GA

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4
Q

How is alveolar surfactant recycled?

A

up to 90% of surf is recycled from the alveolar space; it is broken down via macrophages and/ or reabsorbed into glomerular structures of the type 2 cells

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5
Q

What is the alveolar storage capacity of a preterm infant? term?

A

Preterm: estimated to have only 4-5mg/kg at birth; Term: 100mg/kg

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6
Q

What are conditions that can negatively impact surfactant quality and production?

A

hyperinsulinism, acidosis and MAS (the chemical pneumonitis that occurs with MAS is thought to be the culprit)

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7
Q

what is the function of surfactant in the lungs?

A

inc pulmonary compliance, dec surface tension, facilitates recruitment of collapsed airways, protection of the pulmonary epithelium and prevents atelectasis at the end of expiration

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8
Q

What is pulmonary compliance?

A

the ability of the lung and thorax to expand

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9
Q

Research supports the administration of exogneous surf with what correlated results?

A

a rapid improvement in oxygenation, decrease need for mech vent support, demonstrated an inc in FRC followed by a slower increase in lung compliance, a dec in VQ mismatch

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10
Q

what is the normal surface tension of water v the lung?

A

water: 70 d/cm, the lung is 25d/cm

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11
Q

How does surf fx play a vital role in expiration?

A

at the end of expiration compressed surf phospholipid molecules decrease the surface tension to a very low near zero level. Pulm surf greatly reduces the surface tension (resisting the pull to collapse), inc compliance therefore allowing the lungs to inflate more easily and decrease total WOB

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12
Q

How does alveolar size affect surf?

A

as the alveoli increase in size, the surfactant becomes evenly distributed; this also helps all alveoli in the lungs to expand at the same rate

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13
Q

How does surf keep airways ‘dry’?

A

surface tension forces also draw fluid from the capillaries to the alveolar spaces. by reducing the surface tension, the fluid from the capillaries is not drawn into the alveolar space.

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14
Q

what is the composition of surf?

A

40% dipalmitoylphosphatidycholine (DPPC)
40% other phospholipids
5% surfactant associated proteins (SP- A, B, C, D) cholesterol (neutral lipid)
traces of other substances

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15
Q

What is the strongest phosopholipid in the pulmonary surf mixture?

A

DPPC

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16
Q

What are disease states r/t pulmonary surfactant deficiency?

A

RDS, congenital surfactant deficiencey and pulmonary alveolar proteinosis

17
Q

Can surf be utilized with MAS pts?

A

yes; the mec inhibits the surf fx leading to alveolar collapse, the chemical pneumonoitis and acidosis that also accompanies MAS also may have negative effects on surf

18
Q

Can surf be utilized in patients with pulmonary hemorrhage or pneumonia?

A

maybe; routine use of surf in these two conditions is not recommended, efficacy is uncertain but may still be utilized in clinical practice

19
Q

What are the different types of exogenous surfactant?

A

Synthetic, animal derived and human amniotic fluid derived surfactant

20
Q

what is synthetic surfactant?

A

Exosurf; may or may not have protein components

21
Q

what are animal derived surfactants?

A

Curosurf- extracted from minced pig lung; Infasurf- extracted from calf lung lavage fluid; Survanta- extracted from minced cow lung with additional DPPC, palmitic acid and tripalmitin

22
Q

What is the doseage and administration recommendations for exogenous surf?

A

doseage depends on type of surf given; admin via ETT although some discussion in the lit about via LMA (avoids complications of intubation- has yet to be studied in large randomized trials)

23
Q

What is the weight requirement for LMA use?

A

> 1500 g

24
Q

In clinical practice when is exogenous surfactant administration indicated?

A

persistent worsening respiratory dysfunction, RDS; there should be a low threshold for repeat dosing with RDS patients with perinatal depression or infix. B/c surf is rapidly metabolized and there is a functional inactivation due to soluble proteins in the small airways and alveoli subsequent doses may be req’d

25
Q

WIth exogenous surfactant administration, what monitoring should be done?

A

ETT patency and position
oxygen saturations, EKG and BP (continuously)
-monitor for postdose hyperoxia, hypocarbia and overventilation
s/s blocked airway

26
Q

What are signs that a patient is not tolerating exogenous surf admin?

A

if pt becomes dusky, agitated, bradys, O2 sats decreased by >15% or reflux of surf into the ETT

Dosing should then be slowed or stopped. May require inc FiO2 or ∆ vent settings (inc airway pressure)

27
Q

What can result from postdose over ventilation, hyperoxia and hypocarbia?

A

pneumothorax

28
Q

What percentage of patients given exogenous surfactant experience a pulmonary hemorrhage?

A

2-4%

29
Q

What type of patients given exogenous surfactant are at an increased risk for a pulmonary hemorrhage?

A

primarily in small patients with an untreated PDA; may be due to hemorrhagic pulmonary edema due to a rapid fall in pulmonary vascular resistance and results in inc pulmonary blood flow; more likely to occur in animal derived surf

30
Q

Patients who develop pulmonary hemorrhage from exogenous surfactant administration are more at risk for what?

A

death and short term morbidity