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Clinical Medicine - Pulmonary > RDS > Flashcards

RDS Flashcards

1
Q

Etiology of Respiratory Distress

A 
Respiratory Distress Syndrome (surfactant def.)
Airleak
Meconium Aspiration Syndrome
Neonatal Pneumonia
Pulmonary Hemorrhage
Transient tachypnea
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2
Q

RDS is caused by ..
Usually seen in who ..
Leads to …

A

Caused by deficiency of surface-active material (surfactant) at the alveolar air-liquid interface

Usually in premature babies

Leads to poorly compliant lungs, atelectasis, an increased work of breathing, and hypoxia

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3
Q

At 29 weeks gestational age, what % will have RDS?

A

60%

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4
Q

Basic pathways for surfactant metabolism

A

Surfactant is synthesized in type II cells, stored in lamellar bodies, and secreted into the alveoli where it forms a surface film.

It is cleared from the airspaces by macrophages for catabolism or is taken back into type II cells where it is reprocessed and resecreted, a recycling pathway.

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5
Q

Risk factors for RDS

A 
IDM, fetal hyperinsulinism impedes surfactant production
Fetal asphyxia
Multiple gestation
Males>females
Caucasian>African-Americans
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6
Q

What are the 5 main phases of embryonic lung development?

Which phases are important for conducting airways? terminal respiratory units?

A 
Embryonic
Pseudoglandular
Canalicular
Terminal Sac
Alveolar

1,2 - conducting airways
3,4,5 - terminal respiratory units

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7
Q

Embryonic Period of Lung Development

A

0 - 6 weeks gestation

proximal airways: bronchi

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8
Q

Glandular Period of Lung Development

A

7 - 16 weeks

  • -conducting airways: terminal bronchioles
  • -branching pattern: represents permanent branching pattern
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9
Q

Canalicular Period of Lung Development

A

17 - 25 weeks

  • -acini, gas exchange unit of lung associated with single terminal bronchiole
  • -Respiratory Bronchiole, Alveolar Duct & Sac
  • -full complement of 25,000 terminal bronchioles should be present by 27 weeks
  • -Type II alveolar cells present at 20 weeks
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10
Q

What do Type II alveolar cells do?

A

Produce surfactant

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11
Q

What do Type I alveolar cells do?

A

Gas exchange

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12
Q

Terminal Sac period/Subsaccular phase of lung development

A

25 -35 weeks
primitive alveoli, subsaccules, appear

  • -decrease thickness of interstitium, thinning of epithelium & beginning of septation of terminal air units
  • -increase in alveoli, lung volume & surface area indicate the anatomic potential for gas exchange
  • -Type I & Type II cells differentiate
    • –enlargement of gas exchange surface
  • -lamellar bodies develop, increase in size & number
    • –increase storage of surfactant lipids
  • -Exponential increase in lung volume and surface area as the primitive alveoli appear
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13
Q

Alveolar period of lung development

A

36 weeks - 3 years old

  • -50 million alveoli at term; 300 million at 3 years
  • -Area increase from 3-4 m2 to 75-100m2 by adult
  • -invagination of terminal saccules & formation of secondary protrusions
  • -protrusions elongate & thin forming alveoli
    • –volume of potential air space increases
    • –continued differentiation of Type II cells
  • -collagen synthesis -provides strength
  • -elastin accumulation - provides distensibility
  • -Further thinning of interstitium
  • -appearance of a single capillary network in which one capillary bulges into the lumen of both alveoli with which it is affiliated
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14
Q

What is surfactant composed of?

A 
Saturated phosphatidylcholine (50%)
Unsaturated phosphatidylcholine (20%)
Neutral lipids (8%)
Phosphatidylglycerol
Other phospholipids
Surfactant proteins

Most tests today are based on PC which appears at 28 weeks of gestation

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15
Q

Surfactant Synthesis

A
  • -Surfactant phospholipids synthesized in smooth e.r. of Type II Alveolar Cells (10% of lung surface area)
  • -packaged by Golgi apparatus; stored as Lamellar Bodies
  • -secreted by exocytosis
  • -converted to tubular myelin
  • -rapid provision of phospholipid monolayer to surface interface
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16
Q

Surfactant Proteins: SP-A, SP-B, SP-C, SP-D

–what is their role?

A
  • -Enhance the spreading and stability of phospholipid films.
  • -Determine the structure of surfactant in lamellar bodies and tubular myelin.
  • -Regulate surfactant phospholipid homeostasis.
  • -Regulate innate host defense.
17
Q

What substances are helpful/important in surfactant development?

A

Corticosteroid and thyroid hormones have a regulatory role

Circulating catecholamines stimulate surfactant secretion during labor and birth

Lung distention after birth stimulates surfactant secretion

18
Q

SP-A deficiency

A

Forms integral part of tubular myelin (SP-B required)
Inhibits surfactant secretion but stimulates reutilization
May have a role in determining surfactant pool size
Host defense – opsonization, viral pathogen protection
SP-A Null Mice: Lung inflammation, no tubular myelin

19
Q

SP-D deficiency

A

Innate host defense - viral
Surfactant lipid homeostasis
Protection from oxidant injury
SP-D Null Mice: Altered surfactant homeostais-( pool size) & Viral infections

20
Q

SP-B deficiency

A

MOST IMPORTANT PROTEIN IN SURFACTANT

Surface tension reduction (Accelerate adsorption of phospholipid to air-fluid interface)
Formation of mature lamellar bodies
Formation of Tubular myelin
SP- A needed and enhances ability to reduce surface tension
Genetic defect – Alveolar proteinosis

21
Q

SP-C deficiency

A

Surface adsorption of phospholipids

SP-C Null Mice: minimal effect

22
Q

What agents inhibit surfactant function?

A 
Albumin
Amniotic Fluid
Bilirubin
Cholesterol
Elastin
Fibrin Monomers
Fibrinogen
Hemoglobin
Immunoglobulins
Meconium
Plasma/serum
RBC membrane
23
Q

Laplace’s Law

A

P = 2T / r

  • -models a single alveoli as a perfect sphere
  • -Pressure required to keep alveoli distended is directly proportional to surface tension (T) and inversely proportional to the alveolar radius ( r )
24
Q

How does surfactant work?

A

Aggregate at surface of alveolar lining liquid

REDUCE SURFACE TENSION by displacing water molecules

Surfactant lowers surface tension to near zero (as more water is displaced from the monolayer) and allows for the smallest of alveoli to remain distended at full lung deflation

THUS: surface area is maximized for gas exchange throughout the respiratory cycle

25
Q

RDS pathogenesis regarding surfactant

A
  • -deficient surfactant at air-fluid interface of alveoli in immature lungs
  • -problem with secretion not with synthesis
  • -Deficiency leads to areas of atelectasis
  • -Other alveoli over distend (when on ventilator) and epithelial damage occurs & proteins leak into the airspace further impairing surfactant function
    • –the protein that leaks is what gives the hyaline membrane
26
Q

Summarize the problems that result from RDS

A 
poor alveolar stability
right-to-left shunting of blood
reduced effective pulmonary blood flow
pulmonary edema
hyaline membrane development
reduced lung compliance
27
Q

Clinical manifestations of RDS

A
  • -premature infants
  • -tachypnea, central cyanosis, labored breathing: retractions, flaring and grunting
  • -auscultation may reveal fine rales
28
Q

What does grunting do?

A

Grunting is caused by partial closure of the glottis during exhalation to prevent alveolar collapse
–this increases the pressure

29
Q

Laboratory findings with RDS

A

Laboratory: hypoxia, hypercarbia, acidosis

30
Q

Radiographic findings with RDS

A

Radiographic
granular densities appear within hours of birth
‘ground glass’ appearance

31
Q

RDS prevention

A

Reduce premature births

Predict pregnancies at risk ( 24-34 weeks gestation, intact membranes and impending delivery) and treat with antenatal glucocorticord hormones

Prophylactic/Early treatment of high risk infants (<30 weeks gestation) with exogenous surfactant in delivery room

32
Q

RDS Treatment

A

Resuscitation by skilled team

Intratracheal administration of exogenous surfactant

Meticulous neonatal care (thermal neutrality, infection control, nutrition, fluids)

Assisted ventilation

33
Q

Prognosis of RDS

A

Survival is directly related to birth weight and gestational age, and is affected by the above measures of prevention and treatment.

Long term prognosis for most is excellent: 85-90% are normal.

Clinical Medicine - Pulmonary (8 decks)

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