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NGD > Fetal-newborn transition > Flashcards

Fetal-newborn transition Flashcards

1
Q

Requirements for cardiorespiratory transition

A 
structural maturity of lung
replacement of fetal lung fluid --> air
adequate pulmonary surfactant
onset of breathing
incrase in pulmonary blood flow
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2
Q

Embryonic maturity of lung

A

less than 5 weeks
trachea and bronchi
evidence of 5 lobes

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3
Q

Pseudoglandular lung

A

5-16 wks
airway branching x 15 generations
cuboidal cell lining

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4
Q

Canalicular lung

A

16-25 wks
airways enlarge
thinned epithelium
capillary development

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5
Q

Saccular lung

A

24-36 wks
basement membranes fuse –> future blood-gas barrier
type II cells –> surfactant

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6
Q

Alveolar lung

A

36 weeks to 2-8 years
capillaries bulge into terminal sacs
formation of septae, crests
increasing surface area

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7
Q

Immature lung histology

A

canalicular
thick blood-gas barrier
small area for gas exchange
poorly vascularized

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8
Q

Mature lung histology

A

thin blood-gas barrier
large area for gas exchange
highly vascular

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9
Q

In utero lung fluid

A

ultrafiltrate of pulmonary capillary blood
actively secrete (Cl ion transport)
250-300 ml/day
essential for fetal respiration and maintenance of FRC

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10
Q

Lung fluid in transition

A

fluid secretions slows in late pregnancy
absorption begins in labour (active transport of Na ions)
vaginal squeeze forces fluid out of lungs (not extremely significant)
cleared by capillaries and lymphatics postnatally
aided by lung distension driving fluid into interstitium

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11
Q

Transient tachypnea of the newborn

A 
Retained fetal lung fluid
increased central vascular markings
hyperaeration
evidence of interstitial/pleural fluid
prominent interlobar fissures
flat diaphragm - hyperinflated lungs
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12
Q

Embryonic maturity of lung

A

less than 5 weeks
5 lobules
trachea and bronchi

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13
Q

Canalicular lung

A

16-25 wks
airways enlarge
thinned epithelium
capillary development

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14
Q

Saccular lung

A

24-36 wks
basement membranes fuse –> future blood-gas barrier
type II cells –> surfactant

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15
Q

Fetal channels

A 
umbilical vein
ductus venosus
foramen ovale
ductus arteriosus
umbilical arteries
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16
Q

Breathing after birth

A

Onset
Reduction in pulmonary vascular resistance: crying
increased lung blood flow
increased pO2 in blood
increased blood to the LA
functional closure of foramen ovale due to LA pressure> RA
Cord clamped - increased SVR, close umbilical vessels
closed DA: usually 24-48h in term infants

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17
Q

Mature lung histology

A

thin blood-gas barrier
large area for gas exchange
highly vascular

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18
Q

In utero lung fluid

A

ultrafiltrate of pulmonary capillary blood
actively secrete (Cl ion transport)
250-300 ml/day
essential for fetal respiration and maintenance of FRC

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19
Q

Lung fluid in transition

A

fluid secretions slows in late pregnancy
absorption begins in labour (active transport of Na ions)
vaginal squeeze forces fluid out of lungs (not extremely significant)
cleared by capillaries and lymphatics postnatally
aided by lung distension driving fluid into interstitium

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20
Q

Cord clamping time

A

Effects on infant from delayed (1-2 min) cord clamping
Higher Hb at 24-48 h
Reduced Fe deficiency at 3-6 mo
increase in phototherapy for neonatal jaundice (more blood, more jaundice)
Preterm infants: reduction in rates of interventricular hemorrhage

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21
Q

Transient tachypnea of the newborn

A 
Retained fetal lung fluid
increased central vascular markings
hyperaeration
evidence of interstitial/pleural fluid
prominent interlobar fissures
flat diaphragm - hyperinflated lungs
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22
Q

Surfactant production

A

by alveolar type II cell

stored in Lamellar body, secreted and then adsorped to alveolar space

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23
Q

Surfactant composition

A

70-80% phospholipids
10% proteins - apoproteins AD immunity, BC hydrophobic membrane proteins that increase the rate at which surfactant spreads over surface
10% neutral lipids - cholesterol

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24
Q

Respiratory distress syndrome

A

preterm infant
tachypnea, retractions, grunting, cyanosis
hypoxia
hypercapnia

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25
Q

Fetal breathing movements

A

rhythmic contarctions of diaphragm associated with movement of small volumes of fluid in fetal airway
1-60 min episodes
increase after each maternal meal
circadian rhythm, increasing at night
related to maternal melatonin concentration
inhibited by acute, severe hypoxia, sedatives, alcohol, PGE2

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26
Q

Onset of breathing at birth

A

breathing becomes regular
mechanisms: sensory/chemical stimuli, removal of placental inhibitor peptide

Baby must overcome:

  • viscosity of lung fluid
  • resistance of lung tissue
  • surface tension at air-liquid interface
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27
Q

Newborn thermal properties

A

Cooler environment

heat loss via conduction, convection, radiation, evaporation

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28
Q

Breathing after birth

A

Onset breathing
Reduction in pulmonary vascular resistance: crying
increased lung blood flow
increased pO2 in blood
increased blood to the LA
functional closure of foramen ovale due to LA pressure> RA
Cord clamped - increased SVR, close umbilical vessels
closed DA: usually 24-48h in term infants

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29
Q

Newborn arterial gases

A 
pO2: 1 h 60 , 24 h 90
O2 sat: 1 h 90, 24 h 98
O2 content, 18 then 20
pCO2 35-45
pH 7.3-7.4transition
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30
Q

Time course of cardiorespiratory transition

A

Seconds: first breath, high transpulmonary pressure, not pink
Minutes: pink, regular breathing, pulmonary blood flow increases, absorption of lung fluid
Hours: rising pO2, FRC established, absorption of FLF, increasing lung compliance, RR40-60
Days: remodelling of pulmonary arteries, further increase in lung compliance

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31
Q

Pseudoglandular lung

A

5-16 wks
airway branching x 15 generations
cuboidal cell lining

32
Q

Cord clamping time

A

Effects on infant from delayed (1-2 min) cord clamping
Higher Hb at 24-48 h
Reduced Fe deficiency at 3-6 mo
increase in phototherapy for neonatal jaundice (more blood, more jaundice)
Preterm infants: reduction in rates of interventricular hemorrhage

33
Q

APGAR heart rate

A

0 absent
1 less than 100, almost always due to lung issues
> 100

34
Q

APGAR respiratory effort

A

0 absent
1 slow, irregular
2 good, crying

35
Q

APGAR muscle tone

A

0 limp
1 some flexion
2 active motion

36
Q

Neonatal hypoglycemia

A

Glucose less than 2.6 mmol/L

37
Q

APGAR colour

A

0 blue/pale
1 body pink, blue extremities
2 all pink

38
Q

Fetus thermal properties

A

0.5C > mother
heat transfer via placenta
suppression of thermogenesis: dont waste energy on heat generation

39
Q

Newborn thermal properties

A

Cooler environment

heat loss via conduction, convection, radiation, evaporation

40
Q

Brown fat

A 
mitochondria rich
sympathetic stimulation:
- hydrolysis of triglyceride
- release of FA, glycerol
- heat generated
41
Q

Cold stress

A

36-36.5

42
Q

Moderate hypothermia

A

32-36

43
Q

severe hypothermia

A

less than 32 C

44
Q

WHO warm chain

A 
warm delivery room
immediate drying
skin to skin contact
breastfeeding
bathing and weighing postponed - recommended not to bathe during first 6 hours
appropriate clothing and bedding
mother and baby together
warm transportation
warm resuscitation
training/awareness raising
45
Q

Fetal metabolism

A

anabolism dominant
90-100kcal/kg/day
glucose, lactate, amino acids
glucose levels 70-80% maternal

46
Q

RDS causes

A

1) surfactant deficiency
2) atelectasis –> V/Q mismatch, hypoventilation
3) hypoxemia + hypercarbia –> respiratory + metabolic acidosis
4) pulmonary vasoconstriction –> persistent fetal circulation
5) proteinaceous exudate

47
Q

Symptomatic hypoglycemia

A 
jitteriness, tremor, seizure, coma
irritability, lethargy, stupor
hypotonia, limpness
apnea, cyanotic spells
poor feeding
hypothermia
48
Q

TTN risks

A

precipitous delivery
mtaernal diabetes
maternal sedation
perinatal depression

49
Q

Retractions at birth

A
  • neonates with increased chest wall compliance/reduced lung compliance will have increased negative intrapleural P during inspiration
  • worsening lung compliance before respiratory failure is apparent by blood gas abnormalities
50
Q

Grunting at birth

A

vocal cords partially closed at end of expiration
generates positive end expiratory pressure (PEEP) to stent open small airways, increasing ventilated areas and improving V/Q ratio

51
Q

Head Bobbing at birth

A

Contractions of SCM when accessory muscles in upper thorax are recruited indicating severe respiratory distress

52
Q

DDx neonatal respiratory distress

A 
TTN
RDS
meconium aspiration
non-pulmonary
- anemia, medication, pneumothorax
- congenital heart disease, malformation
- persistent pulmonary HTN
53
Q

aCORN respiratory score

A

Scores 0,1,2
Respiratory rate: 40-60, 60-80, 80
O requirement none, 50
Retractions none, mild-mod, severe
Grunting none, with stimulation, continuous at rest
Breath sounds on ausc: easily heard, decreased, barely heard
Prematurity: >34 w, 30-34, 8 severe

54
Q

Pneumothorax Tx

A

small pneumothorax: often minimally symptomatic
conservative management if not underlying disease, not ventilated, minimal respiratory distress, no continuous leak
Ventilated: minimize pressures (may need to increase rate)
Observe signs of deterioration
Consider 100% Oxygen for nitrogen washout if smaller leaks
Needle aspiration
Chest tube of continuous leak

55
Q

Dx of TTN

A

CXR: hyperinflation, hyperaeration, flat domes of diaphragm, vascular markings in lungs, prominent interlobular fissures
Tachypnea
Intercostal retractions, grunting, nasal flaring: difficulty breathing, low gas exchange
Hypoxia without hypercapnia
Cyanotic

56
Q

Tx TTN

A

self-resolved in 1-3 d
respiratory support and monitoring
O2 requirements usually 4 h, further assessment

57
Q

RDS causes

A

lack of surfactant production/release in alveoli
progressive collapse of terminal bronchiole/alveoli
increased surface tension in alveolus - increased effort for inflation

58
Q

RDS prevalence/popn

A

preterm
male
prenatal depression
maternal diabetes

59
Q

RDS prevention

A

antenatal corticosteroids to increase surfactant production

tocolytic agents potentially arrest preterm labour

60
Q

TTN risks

A

precipitous delivery
mtaernal diabetes
maternal sedation
perinatal depression

61
Q

RDS Dx

A

CXR: ground glass, loss of cardiac silhouette, small lung volume
may see atelectasis
histology: hyaline membranes and collapsed air spaces
tachypnea
intercostal retractions, grunting, nasal flaring, difficulty breathing, low gas exchange
hypoxia with hypercapnia
cyanotic

62
Q

RDS Tx

A

artificial surfactant
varying needs of respiratory support and O2
respiratory distress will worsen if respiratory effort or support unable to prevent progressive lung collapse
fluid and metabolic management

63
Q

Pneumothorax risks

A

aspiration
underlying lung disease
high venitlatory pressures

64
Q

Pneumothorax prevalence/popn

A

primarily in babies with lung disease (aspiration syndromes and RDS) receiving respiratory support, like CPAP or ventilation
spontaneous pneumothorax can occur in 1-2% of health infants during initial spontaneous breaths

65
Q

Pneumothorax Dx

A

present with acute increase in respiratory distress and O2 requirements
Tension pneumothorax may present with sudden onset of CV collapse

66
Q

Pneumothorax Tx

A

small pneumothorax: often minimally symptomatic
conservative management if not underlying disease, not ventilated, minimal respiratory distress, no continuous leak
Ventilated: minimize pressures (may need to increase rate)
Observe signs of deterioration
Consider 100% Oxygen for nitrogen washout if smaller leaks
Needle aspiration
Chest tube of continuous leak

67
Q

Meconium aspiration causes

A

stress during delivery
leads to obstruction of small airways and alveoli
Presents as pneumonitis, disrupts surfactant, mechanical disruption of airway
mechanical obstruction, chemical inflammation, surfactant inactivation

68
Q

Prevalence/popn of meconium aspiration

A

more likely in cases of fetal distress/difficult labour
usually full term infants >34 w
in utero hypoxia, meconium stained amniotic fluid

69
Q

Dx meconium aspiration

A

usually stained amniotic fluid
CXR: atelectasis, consolidation, hyperinflation of lungs/air trapping, spontaneous pneumothorax
audible grunting, severe retractions
may be accompanied by persistent pulmonary HTN of newborn

70
Q

Tx meconium aspiration

A 
severe cases are life-threatening
respiratory ventilator support
manage pulmonary HTN
monitor for pneumothorax
Abx
may need surfactant administration
71
Q

Congenital diaphragmatic hernia causes

A

developmental defect (bowel loops, liver, spleen) in chest cavity

72
Q

Prevalence/popn of congenital diaphragmatic hernia

A

Unilateral: 1/2200 births
80% involve left hemidiaphragm
associated with lethal anomalies (16-22%)

73
Q

Dx congenital diaphragmatic hernia

A

CXR: hypoplastic lungs and obvious defects

wide clinical presentation

74
Q

Tx congenital diaphragmatic hernia

A

surgery

75
Q

Sudden respiratory depression DDx

A 
may occur in intubed baby
DOPE
dislodged
obstruction
pneumothorax
equipment

NGD (16 decks)

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