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Respiratory Medicine > Week 11: Special Respiratory Conditions: Pregnancy, Lung Development and Birth > Flashcards

Week 11: Special Respiratory Conditions: Pregnancy, Lung Development and Birth Flashcards

1
Q

What are the 2 key hormones that increase during pregnancy?

A

Estrogen and progesterone

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2
Q

What is the action of estrogen during pregnancy (both good and bad)

A

increases fluid retention

Good: as it will increase blood volume which will increase delivery of O2 to both baby and mum to ensure that both their metabolic demands are met.

Bad: This fluid retention is bad however as it causes oedema through the airway mucosa and stimulates mucus gland hyperplasia

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3
Q

Comment on the physiological changes that happen to the mother

e.g. Metabolic O2 requirement, physically, and values such as RV, ERV etc.

A
  • The metabolic oxygen requirement increases by about 15 – 30 % above normal (for twins this will be increased)
  • Physically we are going to have compression of the thoracic cavity (due to the growing baby)
  • The diaphragm is going to move up, restricting the ability to inflate the lung
  • Decreased RV
  • Decreased ERV
  • Decreased IRV
  • Decreased FRC
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4
Q

Why when compression of the thoracic cavity, and the diaphragm moving up, will cause decreased RV, FRC, ERV and IRV BUT FEV1 and VC will still not decrease?

A
  • Despite these changes, VC and FEV1 will remain unchanged as the hormonal changes make the ligaments more flexible, widening the subcostal angles, creating a wider and deeper chest cavity (tidal volume gets bigger taking up more of the reserve volumes)
  • Despite this, the energetic cost will go up as the lung as made more stiff
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5
Q

What are the stages of foetal lung development and their time periods

A
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6
Q

Briefly describe what happens in the canalicular and saccular period

A

Canacular all about development of blood vessels

Sacular is when the aveoli sacs develop (first sites of gas exchange develop)

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7
Q

When is surfactant produced during lung development of the baby?

A

inbetween canalicular and saccular period and onwards

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8
Q

During lung development, the foetal lungs are filled with fluid rather than air. What is the role of the fluid?

A
  • This fluid plays an important role in providing a slight positive pressure to the lungs, resulting in lung expansion responsible for stimulating cell division and lung growth.
  • This lung fluid also helps flush out the debris from the lungs (that accumulates from the rapid cell division and cell apoptosis)
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9
Q

Why does the foetus have respiratory movements at the end of the 1st trimester even know it is not actually moving air through its lungs?

A
  • These movements begin to develop the respiratory muscles through moving fluid in and out of the lung and are essential in ‘priming’ or preparing the muscles so that once the baby is born, they are capable of breathing oxygen
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10
Q

Why are the foetal respiratory breathing movements inhibited in the last 7 days?

A
  • It is further important to note that these breathing movements are inhibited in the last 7 days in an effort to prevent the lungs filling with fluid, as well as meconium (foetus poo)
  • If this meconium is inhaled, it can lead to a particularly nasty form of pneumonia that is hard to treat

Also if the lungs are filled with fluid it will make it very hard for the baby to take its first breath.

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11
Q

What is the difference between foetal Hb and adult Hb

A
  • Foetal haemoglobin actually has a higher O2 affinity (left shifted) meaning that it is able to strip oxygens off maternal haemoglobin at the gas exchange site in the placenta
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12
Q

When is foetal Hb replaced with adult Hb?

A

around 6 months of age

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13
Q

What is the first breath of a baby triggered by?

A

thoracic compression via vaginal compression (elastic recoil) rebound of the ribcage then triggers the first breath

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14
Q
  • Most newborns take their first breath within __ seconds, and develop a normal respiratory rhythm within ___ seconds
A

20 seconds, 90 seconds

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15
Q

What are the 2 mechanisms which faciliate clearance of the lung fluid from a foetus?

A
  • The thoracic compression with vaginal delivery will clear some of this fluid
  • The epithelial cells (that produced fluid during embryonic development) also switch to absorption of fluid to assist in the process
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16
Q

Why is it important for the first few expirations of the baby to not be complete? (I.e. why are crying screaming babies a positive sign)

A
  • Crying, screaming babies have a forced expiration
  • This collapses a number of airways causing gas trapping
  • This then facilitates the inflation of the lung

We must not expel all the air, or the alveoli would simply collapse (we want to inflate the air)

  • Over a period of weeks, there will be progressive inflation of the lungs, resulting in higher lung volume, and a significantly diminished required pressure for ventilation
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17
Q

Explain the mechanism of why the alveoli want to collapse?

What is the substance that prevents this from occuring?

A
  • surface tension is generated by the attraction of H2O molecules to each other that lie within the alveolar fluid
  • Specifically, it is the hydrogen molecules that are attracted to each other, this is known as hydrogen bonding or van der Waals forces
  • The net force of all of these hydrogen bonds creates a force that draws into the centre of the alveoli (in the diagram below, the centre of the bubble) –> makes the alveoli collapse
  • Thus, in order to keep these alveoli, open we use pulmonary surfactant (which basically, gets in the way of the hydrogen bonds, disrupting them and thus reduces the forces drawing the alveoli inwards)
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18
Q

What is pulmonary surfactant mainly made up of and what is the most important one?

A

lipids (90%), proteins and carbohydrates

Most lipids are phospholipids with the most important being DPPC

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19
Q

What are the 5 functions of surfactant?

A
  1. Important in reducing the work of the inflating lung (through reducing surface tension)
  2. Decreases the lungs tendency to collapse (lung collapse is known as atelectasis)
  3. It may play a role in lung defence (particularly surfactant proteins)
  4. It may play a role in phagocytosis of bacteria and virus (surfactant protein component)
  5. It may also assist the mucociliary escalator (protein component)
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20
Q

What are the 4 defects of preterm lungs?

A
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21
Q

Infant Respiratory Distress Is a syndrome that occurs when a baby is born with ____________

The earlier a baby is born, the more likely they are to have ___________

A

underdeveloped lungs

infant respiratory distress syndrome

22
Q

What is the primary cause of IRDS

A
  • The primary cause of IRDS is a lack of alveolar surfactant, which causes a massively increased alveolar surface tension and decreased lung compliance
  • This is not good at all, as a baby that is healthy and born at full term already has a stiff lung. So premature babies have to generate massive pressures to inflate the lung
23
Q

What are the 4 pathologies that babies with IRDS will show in their lungs

A
  • Atelectasis (alveoli collapse)
  • Hyaline membranes (become glassy – rupture very easily)
  • Haemorrhagic oedema in the lung (blood vessels will rupture bleeding in the lungs)
  • Hypoxia (due to reduced oxygen perfusion)
24
Q

What are the 3 things that increased mechanical ventilation can cause?

A
  • Decrease alveolarization
  • Increase interstitial collagen
  • Bronchial smooth muscle deposition

Need to be careful as babies airways are extremely fragile

25
Q

What is a treatment that can be given to pre-term babies with decreased surfactant?

A
  • We have seen improved outcomes when exogenous surfactant is administration, that is giving baby’s synthetic surfactant
  • Exogenous surfactant administration results in;
  • Increased gas exchange
  • Decreased barotrauma
  • Decreased infant mortality
26
Q

What type of babies are non-responsive to surfactant treatment?

A

Babies with these genetic predispositions

babies have genetic conditions where they are deficient in surfactant proteins

27
Q

What are the acute complications of infant respiratory distress syndrome?

A
  1. Pulmonary complications
    - These are going to be to do with damage to the lung incurred by the significant pressures required to inflate it
    - Alveolar rupture (high chance of pneumothorax, interstitial emphysema)
    - Persistent pulmonary hypertension (increases risk of pulmonary haemorrhage
    - Pulmonary haemorrhage
    - Apnoea of prematurity is common
  2. Other
    - Trauma to the vocal cords is common as a result of tracheal intubation
    - Intercranial haemorrhage (increases with mechanical ventilation) (basically strokes)
    - Patent Ductus Arteriosus (areas of the gut rot and die due to hypoxia)
    - Necrotising enterocolitis and / or gastrointestinal perforation (caused by hypoxia to the gut causing it to rot)
28
Q

What are the chronic complications of infant respiratory distress syndrome?

A
  1. Chronic lung disease of prematurity (bronchopulmonary dysplasia)
  2. Retinopathy of prematurity
    - Problems with vision
    - Abnormal blood vessels grow and spread through retina pulling it out of position.
    - Infants ventilated with high levels of O2 are susceptible.
  3. Neurological impairment
    - Due to hypoxia of the brain
  4. Hearing impairment and visual handicap may further compromise development
29
Q

What breathing pattern is common in babies that are born pre-term (before 37 weeks of gestation)

A
  • Cheyne-stokes breathing is common and relatively normal in these babies, and is often a consequence of lung mechanics (babies take a high tidal volume compared to their functional residual capacity)
  • This means that their blood gas levels swing, meaning the brain gets mixed signals causing periodic breathing (Cheyne-stokes breathing)
30
Q

What is SIDS

A
  • Stands for sudden infant death syndrome
  • Is the death of an infant under 1 year of age which remains unexplained even after investigation, clinical history review and autopsy
31
Q

What is the theory for SIDS at the moment?

A
  • High levels of dopamine in the carotid bodies (peripheral chemoreceptors), this decreases the sensitivity of peripheral chemoreceptors to detect hypoxia
  • If a baby then rolls over during sleep, and their airways are occluded, the low hypoxic drive doesn’t rouse them
  • This causes a long apnoea causing death
32
Q

Describe the triple risk model for the 3 reasons which can cause SIDS

A
  1. Vulnerable infant
    - An underlying defect or brain abnormality (particularly in those areas of respiration and heart rate control)
  2. Critical developmental period
    - Is the 1st 6 months of life, when there is rapid growth and changes in homeostatic controls (we cant change this)
    - Some of these changes may actually destabilize the infants internal systems temporarily or periodically
  3. Outside stressors
    - Although these stresses are not believed to single-handedly cause infant death, they may tip the balance of a vulnerable infant
33
Q

For SIDS, describe some of the maternal characteristics, birth characteristics, pregnancy characteristics, family characteristics, postnatal characteristics and time of death which lead to SIDS.

A
34
Q

Which hormones help to stimulate lung growth and maturation? Could they be of value in preventing some of the problems associated with premature birth?

A

Cortisol is injected into pre-term babies before they are delivered so they have increased surfactant production

Also thyroid hormone –> helps with rapid lung maturation

35
Q

which hormone help stimulate lung growth and maturation?

A

Cortisol is injected into pre-term babies beofre they are delivered so they have increased surfactant production

Thyroid hormone also helps in rapid lung maturaiton

36
Q

what is thought to trigger the initiation of breathing in the newborn

A

cooling of the skin

37
Q

why may children of mothers with diabetes mellitus exhibit retarded lung development?

A

High insulin –> insulin inhibits surfactant production

38
Q

what factors may lead to a delay in the initation of breathing?

A

anaestetics, trauma during birth

39
Q

how may hypoxia arise in a newborn?

A

compression of the umbillical cord, premature separation from placenta, excessive uterine contractions or excessive anaestesia

40
Q

what is the reason for the increased effort required for the first breath?

A

a large negative pressure is required to overcome the surface tension created by lung liquid in order to inflate the lung.

41
Q

why do neonates require high respiratory rate?

A

have small lung volumes and therefore each time they breath they get smalla mounts of gas exchange and this is not enough for their metabolic requirements. Therefore need to increase respiratory rate to increase demand.

42
Q

what are the forces of attraction between water molecules?

A

van der waals

43
Q

what is the primary cause of infant respiratory distress syndrome and what is the primary affect associated with the condition?

A

lack of alveolar surfactant –> leads to increase surface tension and decrease lung compliance.

Results in haemorrhagic odema, atelectosis, hyaline (glossy) membranes and hypoxia, decreased surfactant.

44
Q

what respiratory support options are avalible for management of IRDS? what are the associated risks?

A

mechanical ventilation with CPAP or PEEP

need to watch pressures as they can cause decrease alveolarisation, increase interstitial collagen, and bronchial smooth muscle deposition

exogenous surfactant

45
Q

what is bronchopulmonar displasia?

A

form of chronic lung disease

from mechanical ventilation

theory is the harm from the mechanical ventilation increase susceptibilty to asthma and copd

46
Q

what is the difference between periodic breath and apnoea?

A

periodic – cheyne stokes - over hyper and hypo ventilation

apnoea is normal breath with cessation

47
Q

why is periodic breathing common in premature infants?

A

consequence of lung mechanics - VC and FRC are low = significant fluctations in blood gas partial pressures (because Vt is greater proportion of FRC)

48
Q

which risk factors are classed as potentially asyphyxiating. How might these factors lead to asphyxiation in a vulnerable infant?

A

airways are not open enough for adequate airflow and oxygenation

49
Q

which risk factors have been targeted by the SIDS public education campaign?

A

Putting baby on back to sleep

putting them in cardboard box to prevent them from crawling under the cot, and there is not room to put other stuff in like blanket that will cover their head.

50
Q

how may reduced neural control of the upper airways predispose infants to obstructive apnoea? what role may sleeping posture play in this?

A

it increases relaxation of upper airways so when they breath on inspiration you have negative pressure which causes collapse of airway.

sleeping on front would make it easier for babies to suffocate

51
Q

how may sensitivty of the carotid bodies be altered in SIDS victims and what impact may this have?

A

peripheral chemoreceptors dont detect decrease O2 as inhibited by dopamine. Therefore lose hypoxic drive to breath and this leads to hypoxia

Respiratory Medicine (15 decks)

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