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Cardiopulmonary > Paeds Pathophysiology > Flashcards

Paeds Pathophysiology Flashcards

1
Q

what is considered a pre-term baby

A

newborn at ot before 34 weeks gestation

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2
Q

what is a neonate

A

less than 1 month old

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3
Q

what is an infant

A

a child that cannot walk (usually <1yr)

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4
Q

do babies breathe from their nose or mouth

A

-predominantly nose because have to breathe and feed

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5
Q

what is the difference in upper airway in adults v/s babies

A

•Large tongues
•Reasonably high pharynx
•Leads to poor tolerance to obstruction and increased WOB
-Smaller airways than adults

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6
Q

what is the difference in bronchial wall structure in babies

A
  • Cartilage is much less firm than adult

* Upper airway including trachea much more prone to collapse

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7
Q

what is the difference in alveoli in adults v/s babies

A

•Full-term baby has no alveoli
-Alveoli do not develop until 2 months old and children do not have full complement until about 8 years old.
•Terminal respiratory units are called saccules - larger than alveoli.
o Smaller surface area for gas exchange
o Smaller respiratory reserve

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8
Q

what is the difference in contralateral ventilation in adults v/s babies

A
  • contralateral ventilation poorly developed
  • connections between respiratory bronchioles, alveoli and terminal bronchioles are poorly developed until 2 – 3 years old
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9
Q

what are the outcome of poor contralateral ventilation in babies

A
  • Atelectasis: can’t get air distal to secretions/obstruction
  • Distal hyperinflation with infection: can get air distal to secretions/obstruction as airways open on inspiration, but can’t get air out as airways close on expiration. Obstructions such as secretions behave like one-way valves in airways.
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10
Q

what is the difference in ribs in adults v/s babies

A
  • Infant ribs are very soft and compliant
  • Poor fulcrum for accessory respiratory muscles
  • Ribs are horizontal
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11
Q

how do babies ribs change when they start walking

A
  • when infants start walking their body orientation with respect to gravity changes
  • This changes the orientation of their ribs to more oblique, bucket handle, adult-like configuration and enables change in thoracic shape to drive change in negative pressure for breathing
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12
Q

what is the difference in breathing technique in infants

A

• Breathing is predominantly diaphragmmatic
• Infant unable to increase chest volume to same extent as an adult because don’t get as much movement
- no bucket handle and poor accessory muscle length-tension relationship due to soft ribs

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13
Q

how do infants increase their their ventilation

A
  • ventilation = tidal volume * respiratory rate
  • babies cant breathe deeper to increase ventilation
  • hence they increase RR
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14
Q

how is the disphragm different in babies v/s adults

A

• Horizontal angle of insertion of diaphragm + more compliant ribs = less efficient ventilation and more distortion of chest wall shape on inspiration.
• Angle of pull/mechanical advantage decreases in infants
o The infant sucks the chest inward

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15
Q

how is fetal and adult circulation different

A

-foetal lungs do not provide oxygen
-the foetus obtains oxygen and nutrients from placenta therefore blood flow to lungs is to keep lungs alive only as they are not required for gas exchange.
Foetal heart achieves this two ways:
• Foramen ovale: hole between right and left atria
• Ductus arteriosus: duct connecting pulmonary artery and aorta.

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16
Q

how does the foramen ovale close

A

-birthing process assists in closing these holes

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17
Q

how long does it take for foetal heart to develop

A

develops very quickly ~ 18 to 19 days and by day 22 it contracts

18
Q

what are the differences in lung compliance in babies v/s adults

A

• Decreased lung compliance even with good surfactant level
• They need greater changes in pressure to increase volume
• Huge changes in pressure => negative pressure in intrapleural space is so high it literally causes suction
-PEEP is not sufficient.
-Negative pressures being generated are so high get recession – sucks structures inward. Floating ribs, then skin in between ribs, then sternum being sucked in.
• Also ribs are soft and therefore very easy to suck them in.

19
Q

what is the effect of a pathology on WOB in infants

A

• WOB becomes very high very quickly in a baby with a lung problem

  • already need a slightly bigger change in pressure to get change in volume
  • If there are pathologies will increase WOB even more as larger pressure changes are required.
20
Q

control of breathing in infants

A

• Brainstem is immature so control of breathing is not as well established

  • babies have irregular breathing patterns with periods of apnoea (absence of breathing for > 20 seconds)
  • central chemoreceptors which detect changes in pH in CSF as a result of CO2 levels are not as responsive to changes in pH. This is normal.
21
Q

how does REM sleep differ in babies

A

-Rapid Eye Movement (REM) sleep
• Neonates sleep up to 20 hours/day
• 80% of sleep time is in REM sleep (cf adults ~ 20%)

22
Q

how does REM sleep affect breathing

A

• During REM sleep lose skeletal muscle tone so there is a reduction in rib cage contribution to breathing

  • Babies spending 80% of their time in REM sleep, also have a less mechanically efficient diaphragm
  • During REM sleep WOB is transferred to diaphragm
  • tend to see laboured breathing, FRC drops, prolonged period of apnoea. This is all normal!
23
Q

what is the mechanical disadvantage for diaphragm in babies

A

o When baby is asleep diaphragm is doing all the work

  • only 25% of fibres in diaphragm are Type I fatigue-resistant.
  • Therefore more likely to fatigue especially with pathology/neurological impairment therefore much quicker regression to respiratory distress
24
Q

what is the difference in metabolic rate in neonates

A

• Much higher demand for Oxygen.

  • VO2 with a neonate 40% is taken up by breathing
  • When sick they will crash really quickly and progress to hypoxemia more rapidly than an adult.
25
Q

difference in ventilation in neonates

A
  • Greater in non-dependent lung/regions
  • Always in a state of V/Q mismatch!
  • Positioning sick babies: on their tummies gas exchange is improved BUT only for TREATMENT in HOSPITAL for a baby being MONITORED – tummy sleeping is associated with SIDS. At home ALWAYS sleep on backs.
26
Q

difference in lung volumes in babies

A

• Smaller VT (tidal volume) because of diaphragm and ribs.

27
Q

foetal Hb difference

A

• Higher affinity for oxygen

- Blood leaving placenta has a higher concentration of O2 than maternal blood.

28
Q

difference in airway protection in pre term babies

A

• will not have a normal cough or gag reflex therefore at much higher risk of aspiration.

  • Spending all their time in supine.
  • Pre-term have anatomical and physiological embryological and surfactant
  • Very stiff, very non compliant, high WOB, high risk of aspiration because of poor cough and gag reflexes.
29
Q

temperature regulation in babies

A

• Infant’s bodies have large surface area to volume ratio.

  • Do not have a fully developed central heat controlling mechanism
  • first couple of weeks babies lose a bit of weight
30
Q

when does lung development begin

A

3 weeks gestation

-rarely complete before 34 weeks

31
Q

what are the 4 stages of lung development

A 
o	Embryonic (wk 3 – 5)
o	Pseudoglandular (wk 6 – 16)
o	Cannalicular (wk 17 – 24)
o	Terminal sac (wk 24 – term)
32
Q

when does terminal sac stage begin

A

-terminal sac stage–> increase in vasculature and production of surfactant starts
-begins at 24 weeks, continues till parturition
o Inability to produce surfactant is the main reason for pre-term infant mortality
o Type I cells -> gas exchange (95%)
o Type II cells -> surfactant (5%)

33
Q

what are the implications for pre-term infants for surfactant

A

 Makes alveoli compliant
 Decreases surface tension of the fluid lining of alveoli
 Promotes alveolar stability – behave as a stable sphere and are less prone to collapse
 Maintains a wet atmosphere (fluid level) to facilitate gas diffusion
 Therefore, decreased surfactant makes alveoli stiff (less compliant) and fluid floods into alveoli (surfactant decreases oedema in alveoli)

34
Q

when is the surfactant well established

A

• Surfactant well established by 30 weeks and production accelerated during labour from chest wall squeeze from passage through the birth canal.

35
Q

what are some signs of resp. distress in paeds pt

A
  • Tachypnoea
  • Use of primitive accessory muscles – nostril flaring
  • Retraction of ribs and sternum - negative pressures in intrapleural space become so negative that they suck structures inward
  • Wheeze - airways narrowing down, more apparent, more quickly and on inspiration and expiration
  • Respiratory grunting – adduct vocal chords in an attempt to produce PEEP to keep airways open for longer to overcome resistance – gets high (and WOB gets high)
  • Cyanosis
  • Sweating
  • Restlessness
36
Q

why are babies at a Higher risk for atelectasis

A

• Smaller alveoli

  • lack of collateral ventilation
  • end up with alveoli distal to secretions collapsing
  • if air can get past secretions during inspiration but can’t get the air out because airways have closed -> hyperinflation
37
Q

why do babies hae high resistance to airflow

A
  • Smaller diameter of airways
  • Distal growth of airways lags slightly behind proximal
  • Even with good matching of capillaries and airways and alveoli. More exacerbated with pre-term baby.
38
Q

why are babies at a high risk of V/Q mismatch

A
  • Less alveoli = less SA for gas exchange
  • Ventilation preferentially distributed to non-dependent lung regions
  • Perfusion preferentially distributed to dependent lung regions – gravity
39
Q

what are the effect of minor insult to breathing n babies

A
  • major increase in WOB
    • Baby with a cold sounds snuffly, high WOB (increase in resistance) and noisy breathing (inflammation closes airways down)
40
Q

what are normal newborn vitals range

A

Heart rate = 130 – 150 bpm
Breathing rate = 35 – 50 per minute
Blood pressure = 60/40 to 70/45 mmHg

Cardiopulmonary (4 decks)

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