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Principles III > Anatomic and physiologic development in pediatric anesthesia > Flashcards

Anatomic and physiologic development in pediatric anesthesia Flashcards

1
Q

When does organogenesis take place and why is this important?

A

First 8 weeks of pregnancy, important because injury during this time causes abnormal organ development

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2
Q

When does organ function develop in a fetus and why is this important?

A

2nd trimester, injury during this time causes abnormal function of organs

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3
Q

When does a fetus gain weight and why is this important?

A

during the 3rd trimester so injury during this time results in reduced fat/organmuscle mass

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4
Q

When can genetic malformations occur in a fetus?

A

At any time

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5
Q

Why is important to ask a mom about her pregnancy?

A

To determine if the fetus/baby had injury during any time that would impair organ function, growth, etc.

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6
Q

Are the lungs in use during fetal circulation?

A

No

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7
Q

What is the path of oxygenated blood to the fetus?

A

Placenta/umbilical vein –> ductus venosus –> IVC –> RA –
> blood preferentially directed across foramen ovale (bypasses pulmonary circulation) –> LA –> LV –> ascending aorta –> brain

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8
Q

What is the path of deoxygenated blood from the fetus to the mother?

A

SVC –> RA –> RV –> pulmonary artery –> ductus arteriosus –> aorta –> umbilical arteries

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9
Q

What is the PaO2 of oxygenated blood delivered to the fetus from mom?

A

80 mmHg

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10
Q

What is the PaO2 of deoxygenated blood delivered from the fetus to the mom?

A

55 mmHg

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11
Q

What changes occur to the pulmonary vasculature at birth?

A

When infant breaths for the first time there is a decrease in PVR as a result of mechanical effects on the vessels and relaxation of vasomotor tone

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12
Q

What circulatory changes happen in the heart of the fetus at birth?

A

as PVR decreases, blood flow increases to the lungs then blood flow into the LA increases via the pulmonary veins which increases LA pressure and closes the atrial septum over the foramen ovale

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13
Q

What does clamping of the placenta do to the infant’s circulation?

A

Clamp of placenta ceases flow form large, low-resistance vascular bed which results in an increase in SVR and decrease in IVC blood flow and RA pressure, increase in SVR and aortic pressure above the pulmonary artery pressure results in reverse flow through the ductus arteriosus

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14
Q

What other factor causes the ductus arteriosus to close?

A

increase in O2 concentration leads to a decrease in prostaglandins

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15
Q

How long does it take for the PDA to close?

A

Shunt can persist for some hours after birth but permanent closure is usually complete 5-7 days but may persist until 3 weeks

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16
Q

When does functional closure of the PDA occur?

A

immediately after birth

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17
Q

When does anatomic closure of the PDA occur?

A

2-3 weeks

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18
Q

What also causes contraction and “functional” closure of the PDA?

A

Increased O2 tensions

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19
Q

Why might some elective cases be delayed for at least a month after birth?

A

To ensure PFO and PDA closes

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20
Q

During birth, what events happen to change fetal circulation to adult-like circulation?

A
  • placenta removed from circulation
  • lungs expand
  • PVR decreases/SVR increases
  • Blood becomes oxygenated through the lungs
  • Portal blood pressure falls
  • Ductus arteriosus closes
  • Foramen ovale closes
  • Ductus venosus closes
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21
Q

What is transitional circulation in infants and when does it occur?

A

Critical period when an infant can readily revert from adult circulation to fetal type circulation, possible during early neonatal period

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22
Q

Why is hypoxia a precursor for transitional circulation?

A

increases PVR which can cause foramen ovale to re-open and the ductus arteriosus may re-open causing a significant portion of blood to bypass the lungs causing rapid desaturation, impaired tissue oxygenation, acidosis, and more increase in PVR…

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23
Q

What are risk factors for prolonged transitional circulation?

A 
prematurity
infection
hypoxia
acidosis
pulmonary disease
hypothermia
congenital heart disease
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24
Q

What can acidosis and/or hypoxia cause during the 1st days of life?

A
  • Prevention of permanent adult-like circulation changes
  • Reversal of adult-like circulation = return to fetal circulation patterns (opening of PDA or LFO)
  • Pulmonary hypertension
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25
Q

What is different about an infant’s myocardial tissue compared to adults?

A

60% is non-contractile tissue where adults only have 30% as non-contractile tissue

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26
Q

What is different about infant’s cardiac output and stroke volume compared to adults?

A

Stroke volume is fixed due to noncompliant and poorly developed L ventricle which then causes cardiac output to be very dependent on HR

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27
Q

What is the hallmark sign of hypovolemic in infants?

A

hypotension WITHOUT tachycardia (due to fixed stroke volume)

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28
Q

What is different in infants’ vagal tone and response to catecholamines?

A

High vagal tone and blunted response to catecholamines

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29
Q

What are some cardiovascular anesthetic implications?

A
  • Sensitive to volume overload
  • Sensitive to myocardial depressants (inhalational anesthetics)
  • Reduced calcium stores (immature sarcoplasmic reticulum)
  • Prone to bradycardia (can be caused by hypoxia, vagal stimulation, volatiles)
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30
Q

What should you do if bradycardia occurs?

A

Rule out hypoxia first and consider anticholinergic if bradycardia is severe and symptomatic

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31
Q

What is the formula to determine normal SBP in pediatrics?

A

90 + (3 x age in years)

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32
Q

What is the formula to determine normal DBP in pediatrics?

A

50 + (1.5 x age in years)

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33
Q

When is extrauterine life possible due to lung maturation?

A

24-25 weeks

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34
Q

At what gestational age does surfactant production begin?

A

22 weeks

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35
Q

At what gestational week do pulmonary capillaries form immature alveolar epithelium?

A

24 weeks

36
Q

At what gestational week do cuboidal alveolar epithelium flatten out and production of surfactant continues?

A

30 weeks

37
Q

What is the purpose of surfactant?

A

Stabilizes alveoli preventing their collapse on expiration

38
Q

What is the principal surfactant and where is it produced?

A

lecithin, produced by type II pneumocytes

39
Q

When does lecithin start being produced and when does production increase drastically?

A

Starts at 22 weeks gestation and increases sharply at 35-36 weeks

40
Q

How is fluid eliminated from the lungs during birth?

A

about 90 mLs of fluid is forced from the lungs during the “vaginal squeeze”, infants delivered by C-section may have more residual fluid in the lungs

41
Q

Why do infants have weak intercostal and diaphragmatic musculature?

A

low numbers of type I muscle fibers (marathon muscles, slow twitch muscles, used for prolonged activity, do not develop adequate type I until >6-8 months

42
Q

What is different about infants’ chest walls?

A

more horizontal and pliable which causes minimal verticle movement and decreased room for lung expansion, results in early fatigue and propensity for apnea

43
Q

What is different about infants’ oxygen consumption?

A

2-3 times higher than adults

44
Q

What is different about infants’ minute ventilation?

A

respiratory rate elevated but TV/kg remains constant throughout development

45
Q

What is different about infants’ airways?

A

Smaller airways that have increased resistance to flow

46
Q

What is different about infants’ FRC and closing capacities?

A

decreased FRC (due to higher metabolic rate and anatomic differences) which causes a decreased closing capacity

47
Q

Do infants have mature hypoxia and hypercapnic drives?

A

No

48
Q

What parts of the central nervous system are immature in infants?

A
  • myelination of nerve fibers is incomplete
  • cerebral cortex less developed
  • BBB immature rendering developing brain more vulnerable to drugs or toxins
49
Q

Do fetuses have behavioral responses to pain in utero?

A

Yes

50
Q

What are potential consequences from neonates have more fragile cerebral vessels?

A 
intraventricular hemorrhage (IVH)
cerebral autoregulation impaired so blood flow is pressure dependent
51
Q

What are predisposing factors to IVH?

A

hypoxia, hypercarbia, hypernatremia, fluctuations in pressure, low HCT, over transfusion, rapid administration of hypertonic fluids

52
Q

What is retinopathy of prematurity (ROP)?

A

arrest of normal retinal vascular development in exchange for retinal vessel proliferation, fibrous tissue formation, and retinal detachment

53
Q

What can cause retinopathy of prematurity?

A

multifactorial, but common in neonates

54
Q

How can you help prevent retinopathy of prematurity?

A

avoid fluctuations in supplemental oxygen, hyperoxygenation, and maintain O2 saturation around 90-95%

55
Q

When do infants’ retinas usually stop developing?

A

42-44 weeks gestation

56
Q

What is periodic breathing?

A

Rapid ventilation with periods of 5-10 second apnea that occurs in preterm infants and some full-term infants

57
Q

What is associated with periodic breathing?

A

increased peripheral chemoreceptor activity to PaCO2

58
Q

When does periodic breathing usually cease?

A

44-46 weeks post conceptual age

59
Q

What is the definition of apnea in infants?

A

no breath for >20-30 seconds

60
Q

What usually accompanies apnea?

A

bradycardia

61
Q

What is the pathogenesis of apnea?

A

Not fully understood

62
Q

Who is most at risk for apnea?

A

Preterm and former preterm infants up to 60 weeks post-conceptual age

63
Q

What are some anesthetic implications to use in an infant that is at high risk for apnea?

A

Admit them for monitoring overnight
Stimulation
CPAP
Caffeine 10 mg/kg IV

64
Q

What is the main oxygen transport protein in the human fetus during developing in utero and persists until roughly 6 months of age?

A

Fetal hemoglobin (HbF)

65
Q

What is different about fetal hemoglobin?

A

Able to bind oxygen with greater affinity than adult Hgb which allows the mother’s oxygen to be delivered across the placenta

66
Q

How does fetal Hgb affect the oxygen-Hgb dissociation curve?

A

Shifts it to the left since it has a higher affinity for oxygen

67
Q

Why is physiologic anemia in infants?

A

During the first 6 months of life adult Hgb synthesis is activated and fetal hemoglobin synthesis is deactivated, in healthy term infants, Hgb levels begin to decline around the 3rd week of life, nadir of physiologic anemia may be as low as 10-11 g/dL at 6-8 weeks of age

premature infants have slightly lower Hgb levels at birth, nadir is lower and reached sooner, avg nadir 7-9 g/dL and reached at 4-6 weeks of age

68
Q

What is a transfusion goal for infants?

A

> 30%

69
Q

Why are pediatric patients at an increased risk for heat loss?

A

larger surface area per kg, thin skin, lower fat content, and higher surface area

70
Q

Which route of heat loss is greatest?

A

Radiation (39%)
Convection (34%)
Evaporation (24%)
Conduction (4%)

71
Q

What can hypothermia in a pediatric patient cause?

A 
Delayed awakening from volatile anesthetics
Cardiac instability
Respiratory depression
Increased PVR
Altered drug responses
72
Q

What are heat production mechanisms?

A
  • non-shivering thermogenesis during the first 3 months of life
  • metabolism of brown fat (shivering severely limited in premature infants and thermogenesis is inhibited by volatile anesthetics)
  • crying
  • movement
73
Q

What are some effects of anesthesia on temperature?

A

Volatiles depress the hypothalamus and reduce an already lowered ability to warm themselves

74
Q

What can you do to help prevent hypothermia in pediatrics?

A 
Transport the child in incubator or heating pad
Warm the OR and fluids
Limit skin exposure
Cover the chid's head
Bair huggers and warmers at all times
Heat Lamps
75
Q

When does a child get normal kidney function?

A

not till >6 months, may not achieve until 2 years

76
Q

In utero, is kidney function active or passive?

A

passive, reduced GFR and RBF

at birth transition occurs which increases RBF and GFR

77
Q

How is the ability to concentrate urine changed?

A

limited in 1st 48 hours because of decreased solute gradient for exchange, able to concentrate urine at about 1 month of age

78
Q

How much can the renal system accommodate for large swings in volume?

A

significantly reduced ability to accommodate for large changes in volume

79
Q

When is renal tubular function adult-like?

A

12-24 months

80
Q

How is the renal clearance of drugs different in pediatrics?

A

reduced, ability to handle free water and solute loads may be impaired in neonates, half-life of medications excreted by glomerular filtration will be prolonged

81
Q

When is hepatic maturity complete?

A

Somewhat complete at term

82
Q

What is different about the CYP450 levels?

A

reaches ~50%of adult values at birth, phase II (conjugation making drugs more water soluble for renal excretion) are impaired until ~ 1 year of age

83
Q

What is different about glycogen stores?

A

limited glycogen stores so predisposed to hypoglycemia during stress

84
Q

When are pediatric patients considered hypoglycemic?

A
85
Q

How is calcium homeostasis maintained?

A

in utero actively transported across the placenta, after birth infant relies on calcium reserves however parathyroid function is not fully established and vitamin D stores may be inadequate

86
Q

How should you treat symptomatic hypocalcemia?

A

slow infusion of either calcium chloride or calcium gluconate, central line is preferred as skin damage and sloughing may occur with calcium-containing solutions

Principles III (12 decks)

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