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LC Unit 3 > Adaptation to extrauterine life > Flashcards

Adaptation to extrauterine life Flashcards

1
Q

3 diff phases of lung development

A
  1. Canalicular phase
  2. Saccular phase
  3. Alveolar phase
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2
Q

Canalicular phase

  • weeks
  • Importance
A

17-27 weeks

Delineation of pulmonary acinus

Type II cells begin to differentiate, capillary network begins

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3
Q

Saccular phase

  • weeks
  • Importance
A

26-36 weeks

Thinning of interstitial space, closer association of endothelial and type I cells

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4
Q

Alveolar

  • weeks
  • Importance
A

36 weeks - 3 yrs

Presence of true alveoli

Lengthening and sprouting of capillary network

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5
Q

Surfactant

  • what is it
  • what does it do (4)
A

Phospholipid-protein complex (90% lipid, 10% protein)

Fxn:

  1. Lowers surface tension
  2. prevents alveolar collapse at end expiration
  3. Decreases work of breathing (improves compliance)
  4. Aids host defense

compliance - how ez it is to expand lungs. If you can change a lot of volume with very little effort - more compliant

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6
Q

What happens when you get the wind knocked out of you?

A

lose fxnal residual capacity

- normally, you dont empty your lungs completely

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7
Q

compliance

- Max compliance

A

how ez it is to expand lungs. If you can change a lot of volume with very little effort - more compliant

Max: max lung expansion for min effort

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8
Q

Where is surfactant made and how is it stored? How is it secreted? What does it do after it is secreted into the airspace?

A

Made in type II alveolar cells

  • stored as lamellar bodies
  • secreted as tubular myelin into airspace
  • tubular myelin lines up along air-liquid interface in a multilayer fashion
    (when air space collapses, the tails are densely packed, leading to mutual repulsion, opposing the collapse)

*good image in ppt

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9
Q

Role of surfactant in generating more pressure to get a lot of volume movement.

A

Without surfactant, you have to generate more negative pressure (or positive pressure if you are being ventilated) to move air into lung, to get a lot of volume movement.

Lung becomes poorly compliant. And lung loses FRC (air in lung after exhale)

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10
Q

X ray of surfactant deficiency

A

white out

CXR with diffuse microatelectasis (very poorly aerated)

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11
Q

Importance of FRC

A

Too low: lung underinflated, very noncompliant

Too high: (emphysema) lung over expanded to near lung capacity

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12
Q

Signs of surfactant deficiency aka (Hyaline membrane disease HMD)

A
  1. Premature or delayed maturity
  2. Increased work of breathing
    - retractions
    - grunting, flaring
  3. Cyanosis in room air
  4. CXR with diffuse microatelectasis (very poorly aerated)
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13
Q

Treatment of surfactant deficiency

A

Oxygen

Improve lung inflation, establish FRC

  • continuous PP airway (nasal CPAP)
  • intubation and mechanical ventilation
  • surfactant replacement
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14
Q

Lung fluid absorption

  • what is it
  • what needs to happen at birth
A

In the fetus, lungs are filled with fluid

  • fluid is produced by the lung, comes from trachea, forms amniotic fluid
  • fluid is secreted by lung epithelial cells, driven by active Cl- secretion

At birth, fluid needs to clear quickly to establish ventilation with air
- absorption depends on Na+ absorption

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15
Q

Clearance of fetal lung fluid

- Influence of maturity

A

Presence and activity of amilioride sensitive selective ENaC increase in late gestation, probably due to increased fetal production of cortisol.
- can be induced by exogenous GC and somewhat by catecholamines (stress of labor)

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16
Q

Clearance of fetal lung fluid

- Labor

A

Increased transpulmonary P

  • uterine contractions squeeze fluid out at a greater rate than it is produced
  • if no labor, more fluid remains to be removed after birth
17
Q

At birth, what happens to FRC?

A

It increases a little bit with each effective inspiration

  • but a big first inspiration is necessary to move air liquid interface more distally into air space –> interstitium –> circulation
  • CPAP can help
18
Q

In fetal life, is the flow of fluid bidirectionally?

A

No - always egressing

- ie: meconium aspiration –> inflammatory process

19
Q

Failure of new born to breathe can be a result of:

A
  1. Primary apnea
  2. Secondary apnea
  3. Neuromuscular impairment
20
Q

Primary apnea

A

stimulation (rubbing, drying) easily initiates cry

21
Q

Secondary apnea

  • what is it?
  • When is it assumed?
A

Requires rescue with PPV to estab. lung inflation and begin regular respirations

*at birth, if HR is low and baby is not breathing, we assume its 2ndary apnea and intervene quickly w/ PPV

22
Q

Issues in Neuromuscular impairment in new born making it difficult for them to breath

A

Due to:
- Maternal sedation, analgesia, MgSO4 during labor
- Primary neuromuscular problems in newborn:
myotonic dystrophy, congenital myopathies, SC injury, spinal muscular atrophy

23
Q

At birth, and baby is not breathing, and not breathing when we dry them off, do we assume it will be primary or secondary or neuromuscular impairment related?

A

Secondary apnea

- immediately give PPV

24
Q 
Apgar score:
Max points:
How is it measured:
Does it predict long term outcome?
Does it dx asphyxia?
A

Max points: 10 min
How is it measured:
- assigned at 1 and 5 min
- then every 5 min until 20 min until score is 7

Does it predict long term outcome? No (but

25
Q

Apgar score

measures what categories?

A 
Heart rate
Respiration
Muscle tone
Response to suction
Color

(points are 0-2 for each)

26
Q

How does lung inflation help with cardiovascular transition?

A

Sets stage for ez tidal breathing (FRC)

Resultant increased alveolar oxygen
- decrease pulmonary vascular resistance –>
Increases pulmonary blood flow
- Increased arterial pO2 –> constriction of ductus arteriosus
- Increased pulmonary bf –> increases LA volume –>
closes foramen ovale flap

*LUNG INFLATION IS KEY TO CV TRANSITION

27
Q

Trace flow of blood from placenta to systemic system (brain + heart)

A 
Mom --> 
Placenta -->
Umbilical vein -->
Ductus venosus -->
IVC -->
RA --> 
(because of the way the blood streams into RA, it preferentially shoots thru foramen ovale) --> 
LA -->
LV -->
Ascending aorta -->
Brain + heart
(best oxygenated blood)
- organs most resistant to hypoxic insult
28
Q

Trace flow of blood from fetus body to

placenta

A 
SVC --> 
RA --> 
RV --> 
Pulmonary artery -->
(but since there is a ductus arteriosus that is huge in the fetus and the vascular resistance is high in lungs, and low systemically because placenta is still in systemic circuit, blood goes from pulmonary artery -->
aorta -->
adrenal glands, pancreas (rest of body)
29
Q

Postnatal circulation:

biggest change

A
  1. PLacenta is removed, cord is clamped
    - systemic vascular resistance increases
  2. Body is cold and wet
    - systemic vasoconstriction
  3. Lung expands
    - PVR drops
    - Pulm bf increases
    - PaO2 increases
  4. Ductus arteriosis ad venosis constricts
  5. Venous return from lung increases:
    - Foramen ovale flap closes

*ALL REVERSIBLE

30
Q

Response to delivery:
Umbilical artery

Umbilical vein

A

Umbilical artery
- vasoconstrict with increasing oxygenation

Umbilical vein
- collapse with absent blood flow from (now absent) placenta

31
Q

Response to delivery:
Ductus arteriosis

Ductus venosus

A

Ductus arteriosis
- fxnally closes w/ increased oxygenation and loss of PGE2 from placenta

Ductus venosus
- collapse with absent blood flow

32
Q

Response to delivery:
Foramen ovale

Pulmonary arteries

A

Foramen ovale
- closes when systemic pressure (LA) is > than pulmonary P (RA)

Pulmonary arteries
- vasodilate with elevated oxygen lvls

33
Q

3 birth abnormalities that can cause Persistent pulmonary HTN of newborn (PPHN)

A

abnml:
1. PVR remains elevated
(+/- SVR fails to increase)
2. Blood continues to flow R–>L across foramen ovale
3. Ductus arteriosis remains open, blood cont to flow R –> L (PA to Aorta) and bypassing the lungs

34
Q

Differential oxygenation

A

Pre-ductal blood (head + R arm) well oxygenated

Post ductal blood (descending aorta) is less well oxygenated (mixed)

Similar to PPHN

35
Q

3 main categories of PPHN

A
  1. Abnormally constricted pulmonary vessels
  2. Remodeled pulmonary vascular tree (abnl musculature)
  3. Hypoplastic pulmonary vascular tree
36
Q

Factors that decrease PVR

A

things that cause alveolar distention:

  1. INcrease Po2
  2. INcrease pH
  3. INcrease NO
  4. Increase Prostacyclin
  5. Decrease Pco2
37
Q

Signs of neonatal hypoglycemia

A 
jittery
irritable
lethargy
apnea
seizures

dx: blood sugar

38
Q

Factors that maintain pulmonary vasoconstriction

and increase PVR) (5

A
  1. low pO2
  2. low pH
  3. high pCO2
  4. Leukotrienes
  5. Endothelin
39
Q

Factors that maintain pulmonary vasoconstriction

and increase PVR) (5

A
  1. low pO2
  2. low pH
  3. high pCO2
  4. Leukotrienes
  5. Endothelin

LC Unit 3 (14 decks)

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