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Pediatric Physiology - B. Stevens/Bernstein 2017 > Peds Physiology > Flashcards

Peds Physiology Flashcards

1
Q

Prenatal period or resp development from the 17th week of gestation onwards; branching of the baby’s airways to terminal bronchioles

A

Pseudoglandular period

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2
Q

Prenatal resp development period in which the baby’s airways are branching into the resp bronchioles

A

Canalicular period

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3
Q

Prenatal resp development period in which clusters of terminal air sacs with flattened epithelia are developed

A

Terminal Sac (alveolar) Period

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4
Q

earliest week of gestation a baby can survive outside the mother; what is this period called?

A

24th week gestation

Terminal Sac (alveolar) period

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5
Q

at what week of gestation is proliferation of capillaries around the saccules sufficient for gas exchange?

A

24 weeks

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6
Q

at what week of gestation does alveolar formation begin?

A

32-36 weeks

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7
Q

at birth, does a baby have fully developed alveoli?

A

No. Saccules still predominate at birth

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8
Q

2 roles of lung fluid in prenatal lung development

A

Expands airways, stimulating lung growth

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9
Q

what contributes to 1/3 of total amniotic fluid?

A

lung fluid

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10
Q

amount of pressure needed for a baby to take its first breath

A

40-80 cmH2O

Remember that this is 2-4x the pressure we give to a ventilated pt

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11
Q

Why does a baby’s first breath require high pressures? (2 reasons)

A
  1. to overcome surface tension forces

2. to introduce air into fluid filled lungs

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12
Q

What is essential to enable a baby to take its first breath?

A

Adequate surfactant

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13
Q

What two things are associated with the elevation in PaO2 a baby experiences in the perinatal period?

A
  1. marked increase in LAP

2. Closure of Foramen Ovale

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14
Q
  1. At what week gestation does surfactant production appear in the baby’s lungs?
  2. What cells produce this surfactant?
A
  1. 27 weeks gestation

2. Type II pneumocytes

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15
Q

absence of _______ contributes to RDS in premies

A

surfactant

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16
Q

In a preterm delivery, the administration of betamethasone or dexamethasone to a mother 48h before delivery helps in what 3 ways?

A
  1. accelerates lung maturation
  2. stimulates surfactant production
  3. decreases mortality after 30 weeks gestation
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17
Q

What is produced by Type II pneumocytes?

A

Surfactant (Fun Fact: Whenever a test says type II pneumocytes, surfactant is probably the correct answer)

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18
Q

What ratio in amniotic fluid correlates with lung maturity?

A

Lecithin/sphingomyeliin (L/S) ratio

(Fun Fact: Lecithin and sphingomyelin are 2 components of surfactant. Lecithin makes surfactant more effective. An L:S ratio >2.0-2.5 usually indicates lung maturity)

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19
Q

Equation/Law that applies to surfactant and alveoli. How does it apply?

A

La Place Equation:
P = nT/r

If descending PRESSURE (P) is same in all alveoli and RADII (r) of the alveoli can vary, then wall TENSION (T) in alveoli will vary –> UNSTABLE!!

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20
Q

4 factors that are known to increase the synthesis of surfactant

A
  1. glucocorticoids
  2. thyroxine
  3. Heroin
  4. cAMP
    and other miscellaneous factors
    (Remember that to get more surfactant, you must “Get To Harry’s Camp”)
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21
Q

5 factors known to inactivate surfactant

A
  1. alveolar-capillary leak
  2. pulmonary edema
  3. hemorrhage (hgb)
  4. alveolar cell injury
  5. Meconium**
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22
Q

In what 5 situations would the use of synthetic surfactant be an appropriate tx?

A
  1. Premies with surfactant deficiency
  2. PPHN (persistent pulm HTN)
  3. CDH (congenital diaphragmatic hernia)
  4. Meconium aspiration syndrome
  5. ARDS - adults and kids
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23
Q

Up to what age does lung development continue to occur?

A

10 years

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24
Q

At what age does the number of alveoli stop increasing?

Does the size also stop increasing?

A

8 years

No. Size continues to increase after age 8

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25
Q

At what age have all the saccules developed into alveoli?

A

18 months

Fun Fact: Alv surface area at birth = 2.8 M2, at 8 years = 32 m2, and as adult = 75 M2

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26
Q

Do babies breathe through their nose or mouth?

A

nose, and their nares are narrow

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27
Q

how is a baby’s larynx positioned compared to an adult’s?

A

baby’s is cephalic at C3

Adult’s is C5

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28
Q

3 main differences in a baby/kid’s epiglottis vs adults

A

a kid’s is

  1. narrow
  2. floppy
  3. posteriorly angled
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29
Q
  1. narrowest part of child’s airway until 10 y/o

2. what is unique about that structure?

A
  1. cricoid cartilage
  2. it forms a complete ring

[Fun Fact you should know by now: a kid’s airway is cone-shaped]

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30
Q

3 structures that may result in difficult airway ventilation and visualization in a child

A
  1. large tongue
  2. adenoids
  3. tonsils

[Fun Fact: If a kid obstructs/has sleep apnea at home, they will do it during induction too =) ]

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31
Q

How is the epiglottis shaped in a child?

A

like a U

and it is long

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32
Q

where is the larynx located in a child compared to an adult?
(3 answers)

A
  1. anterior
  2. Cephalad
  3. C4 level
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33
Q

In a neonate, the trachea is short; what is the distance from the cords to the carina?

A

2 cm

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34
Q

13 factors a pre-op airway exam/history should focus on

A
  1. prior difficult intub
  2. prior head, neck, or oral surgery
  3. airway infection
  4. snoring
  5. specific syndromes or diseases
  6. congenital lesions
  7. Laryngeal web, neck mass, hemangioma, subglottic stenosis, laryngomalacia
  8. gross abnormalities
  9. mouth opening and mallampati if possible
  10. prior cleft lip or palate
  11. tongue size, mandibular size and symmetry
  12. neck mobility
  13. ability to cooperate (have fun with that)
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35
Q

4 essential parts of the airway exam that must be completed even on uncooperative children

A
  1. relation of incisors during normal jaw closure
  2. thyromental distance
  3. length of neck
  4. thickness of neck
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36
Q

7 conditions that often include macroglossia and could indicate a difficult airway

A
  1. Trisomy 21
  2. Beckwith-Wiedemann
  3. hurlers
  4. Kocher-Debre-Semel
  5. Ainge
  6. Pompe’s
  7. Grieg’s
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37
Q

11 conditions that often include retrognathia (micrognathia) and could indicate a difficult airway

A
  1. arthrogryposis
  2. Cornelia de Lange
  3. Cri du chat
  4. Dwarfism
  5. DiGeorge
  6. Goldenhar
  7. Klippel-Feil
  8. Pierre Robin
  9. Trecher Collins
  10. Turners
  11. Trisomy 18, 21, 22
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38
Q

4 elements of the respiratory drive

A
  1. central chemoreceptors (H+)
  2. periph chemoreceptors (CO2, pH, O2)
  3. 3 types of neural components
    - Type 1 (glomus) cells
    - Type 2 (sheath) cells
    - sensory nerve fiber endings
  4. neural pathway (CN9)
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39
Q

receptors located near the surface of the ventrolateral medulla whose principal stimulus is H+ ions

A

Central Chemoreceptors

{senses the pH of CSF and interstitial fluid which are readily altered by pCO2]

Response:
increased H+ = increased ventilation

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40
Q

location of peripheral chemoreceptors

A

carotid bodies

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41
Q

which nerve provides the neural pathway for the resp drive

A

carotid nerve from CN IX (Glossopharyngeal)

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42
Q

stimulus and response for the periph chemoreceptors

A

Stimulus:

  1. PaCO2
  2. pH
  3. PaO2 (esp <60 mmHg)

Response:
increased ventilation

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43
Q

How much to peripheral chemoreceptors contribute to the resting ventilatory drive? ____%

A

15%

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44
Q

How does hypoxia affect ventilation in neonates? Why?

A

Hypoxia depresses ventilation in neonates via suppression of medullary centers

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45
Q

What happens in the carotid bodies when a child experiences years of chronic hypoxia (for example from cyanotic CHD)?
Can this effect ever be reversed?

A

The carotid bodies lose their hypoxemic response

Hypoxic response does return upon correction/restoration of normoxia

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46
Q

In the case of chronic respiratory insufficiency with hypercarbia, what becomes the PRIMARY stimulus of the respiratory centers?

A

Hypoxemic stimulus of carotid chemoreceptors

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47
Q

In a patient with chronic resp insufficiency with hypercarbia, what could O2 administration lead to?

A

increased PaCO2 via decreased ventilation (hypoxia is their primary drive to breathe)

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48
Q

How does anesthesia affect the CO2 response curve?

A

the curve shifts right because anesthesia decreases the body’s response to CO2

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49
Q

how does anesthesia affect the pO2 response?

A

anesthetics and opiates lead to MARKED suppression of hypoxic drive

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50
Q

how do anesthetics influence airway patency?

A

anesthetics cause the depression of genioglossus, geniohyoid, and pharyngeal dilators –> upper airway obstruction

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51
Q

In which patient population would you expect to have more difficulty with airway patency after induction of anesthesia? Adults or Infants?

A

Infants

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52
Q

Consider the Hgb-O2 Dissociation curve. Is the Bohr Effect more pronounced in fetal Hgb or Adult Hgb?

A

Fetal Hgb

The Bohr effect is described as: increased CO2 (therefore decreased pH) leads to a decreased affinity of Hbg for O2. This occurs in the tissues. In the case of adult hgb vs fetal hgb, when pO2 is 50 (p50), an adults O2 sat will be 26% but a baby’s O2 sat will only be 19%. This occurs in part because fetal hgb reacts poorly with 2,3-DPG.

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53
Q

In light of the Bohr Effect, how would hyperventilation impact tissue O2 delivery?

A

hyperventilation can cause decreased O2 delivery to tissues (increasing pH (alk) decreases p50)

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54
Q

By 3 mo of age, how does a baby’s p50 compare to that of an adult?
By 9 mo?
Why?

A

3 mo p50 = 27% O2 sat (same as adult)

9 mo p50 = 30% O2 sat

Fetal hgb gets replaced. This does lead to a physiologic anemia so check the kid’s hgb when they come in for surgery.

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55
Q 
If SpO2 = 91%, then PaO2 = 
Adult \_\_\_\_\_
6 mo \_\_\_\_\_
6 wks \_\_\_\_\_
6 hrs \_\_\_\_\_
A

Adult 60 mmHg
6 mo 66 mmHg 6 wks 55 mmHg 6 hrs 41 mmHg

Implication: low sats on a baby require immediate attention

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56
Q

True or False: an older infant tolerates lower Hgb level at which a neonate ought to be transfused.

A

True.

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57
Q

Easy rule of thumb to figure out what normal MAP should be for ages newborn to toddler

A

adequate MAP = gestational age in weeks

58
Q 
Average Pediatric HR (awake and asleep) 
Neonate (96h) \_\_\_\_\_
Infant (6 mo) \_\_\_\_\_
Toddler (2 yr) \_\_\_\_\_
Preschool \_\_\_\_\_
School age (7 yr) \_\_\_\_\_
Adolescent (15 yr) \_\_\_\_\_
A

Neonate:
awake - 100-180
asleep - 80-160

Infant
awake - 100-160
asleep - 75-160

Toddler
awake - 80-110
asleep - 60-90

Preschool
awake - 70-110
asleep - 60-90

School
awake - 65-110
asleep - 60-90

Adolescent
awake - 60-90
asleep - 50-90

59
Q 
Normal RR for peds (awake and asleep)
6 - 12 mo \_\_\_\_\_
1-2 yrs \_\_\_\_\_
2-4 yrs \_\_\_\_\_
4-6 yrs \_\_\_\_\_
6-8 yrs \_\_\_\_\_
teen \_\_\_\_\_
A

6-12 mo
awake - 58-75
asleep - 22-31

1-2 yrs
awake - 30-40
asleep - 17-23

2-4 yrs
awake - 23-42
asleep - 16-25

4-6 yrs
awake - 19-36
asleep - 14-23

6-8 yrs
awake - 15-30
asleep- 13-23

Teen 12-16

60
Q

BP for preschool-adolescents

A

preschool
SBP 96-110
DBP 55-69

school
SBP 97-112
DBP 57-71

adolescent
SBP 112-128
DBP 66-80

61
Q

When is gas exchange first possible in an unborn baby?

A

24 weeks gestation

[ Key point =) ]

62
Q

True or False: Significant development of the resp system continues postnatally.

A

True

[Key point]

63
Q

What is the important resp muscle to developing lungs?

A

Diaphragm

(fewer type 1 fibers (10% vs 25%) when first born)

[Key point]

64
Q

How much do the intercostals contribute to developing lungs?

A

contribution is very limited –> high compliance

[Key Point]

65
Q

Changes in Hgb p50 have implications for _____.

A

Transfusion

[Key Point]

66
Q

What is the implication of a peds pt’s small and limited number of alveoli?

A

decreased lung compliance

67
Q

What is the implication of a peds pt’s cartilaginous rib cage?

A

increased chest wall compliance

68
Q

True or False. Chest is circular shaped with horizontal ribs.

A

True

69
Q

Why is the pediatric diaphragm easily fatigued?

A

It has fewer type 1 muscle cells.

(Fun Fact: There are 2 types of skeletal muscle cells: type 1 (slow twitch) and type 2 (fast twitch). Slow twitch muscles aid in endurance. Fast twitch muscles aid in powerful bursts of movement)

70
Q

Is a baby’s abd must strength fully developed?

A

no.

71
Q

What law describes the increased airway resistance in a pediatric pt?

A

Poiseuille’s Law

72
Q

A pediatric patient has low residual lung volumes at expiration (FRC). The FRC overlaps closing capacity. What does this lead to?

A

atelectasis

73
Q

State 2 reasons why a pediatric patient has an increased O2 consumption. What is their O2 consumption?

A
  1. higher minute ventilation
  2. higher blood flow to vessel rich group

7 mL/kg/min

74
Q

True or False. Hypoxic and hypercapnic respiratory drives are very well developed in a peds pt.

A

False.

75
Q

True or False. A pediatric patient has a large oxygen reserve.

A

False. Oxygen reserve is limited.

76
Q

How long should you want to do an elective surgery on the following patient populations:

  • term infant
  • slightly premature
  • extremely premature
A

Term: 45 weeks

slight preme: 55 weeks

Extreme preme: 65 weeks

77
Q

Apnea of Prematurity occurs in 25% of all pre-term infants and can present as: _____ vs. _____

A

periodic breathing vs. outright apnea

Fun Fact: all premature infants are monitored for apnea of prematurity

78
Q

Define “apnea” in an infant.

A

pause in ventilation lasting >20 seconds

79
Q

Define “periodic breathing” in an infant.

A

aobeuc soaks < 10 seconds without bradycardia or cyanosis

80
Q

Define “central apnea” in an infant.

A 
No initiation of a breath for 
>15 sec or 
<15 sec but associated with
- HR <100
- cyanosis or
- pallor
81
Q

Define “obstructive apnea” in an infant

A

Breaths are initiated without passage of gas d/t airway obstruction

82
Q

Is periodic breathing normal in a baby?

A

Yes.

83
Q

How can periodic breathing be abolished?

A

Add 3% CO2 to inspired gas

84
Q

True or False. Central apnea is rare in full term infants but common in premies.

A

True

85
Q

Locations of obstructions in infants that can lead to obstructive apnea:

A 
Level of obstruction:
- Extrathroacic
- Intrathoracic
Nature of obstruction:
- Intraluminal
- Extrinsic
- Structural
86
Q

Causes of central apnea in infants

A
  • immature control
  • infection
  • CNS process
  • reflux
  • congenital
  • pharmacologic
  • secondary to airway impedance
87
Q

Causes of obstructive apnea in infants

A
  • craniofacial abnormalities
  • enlarged lymphoid tissues
  • pharyngeal hypotonia
  • foreign body
  • airway compression
88
Q

Factors that exacerbate apnea of prematurity

A
  • anesthesia
  • narcotics
  • hypothermia
  • hypoglycemia
  • anemia
  • hyperglycemia

Fun Fact: We do/cause all of this. Yay us.

89
Q

Associated factors that increase risk of post-op apnea in preterm infants (5)

A
  1. extent of surgery
  2. anesthetic technique
  3. anemia
  4. hypoxia
  5. narcotics
90
Q

5 factors that diminish (but not eliminate) apnea of prematurity

A
  1. Caffeine 10 mg/kg IV
  2. Theophylline (little used)
  3. Stimulation
  4. Avoidance of GA (use pure regional if possible)
  5. avoid narcs
91
Q

5 causes of rapid desaturation in pediatric anesthesia

A
  1. low FRC
  2. high O2 requirements (VO2)
  3. shunts
  4. anesthetic technique
  5. patient cooperation
92
Q

2 key concepts related to the rapid desaturation of pediatric pts

A
  1. FRC is the available reservoir of O2 during apnea

2. VO2 reflects the rate that reservoir is depleted

93
Q

This is the Fun Fact card!

Fun Fact #1: FRC = 50% of TLC and may be only 15% of TLC in young infants under GA plus muscle relaxants

A

Fun Fact #2: RV = 25% of TLC in a peds pt

94
Q

Name 2 implications of a smaller FRC/kg in a pediatric pt?

A
  1. the O2 reservoir after preoxygenation is smaller

2. smaller O2 reservoir –> faster desaturation if ventilation is inadequate or nonexistent

95
Q

How long do you have from the onset of apnea to critical desaturation after pre oxygenation in a healthy child?
In a healthy infant?

A

Child: 3 min
Infant: 1 min

96
Q

Common cause of shunts –> rapid desaturation in infancy

A

Patent Foramen Ovale

97
Q

Is a patent Foramen Ovale normal in neonates?

A

Yes

Fun Facts:

  1. Foramen Ovale patency persists for months after birth
  2. 50% of infants have probe patent PFO at 1 yr
  3. 25% of adults have probe patent PFO
98
Q

What causes a PFO to result in a shunt and consequent desaturation?

A

RA pressure > LA pressure

Fun Fact: Normally LA pressure > RA pressure –> flap of foramen ovale closes –> no shunt

99
Q

5 factors that increase PA pressure and therefore RA pressure

A
  1. Hypoxia
  2. Hypercarbia
  3. High airway pressures
  4. Hypothermia
  5. Pain

Remember: increased RAP can lead to R –> L shunting if PFO or other hole is present

100
Q

Which branch of the ANS is dominant in adults? In infants?

A 
adults = sympathetic dominant
infants = parasympathetic dominant
101
Q

Concerning laryngoscopy and hypoxia, what is the result in the difference between the ANS dominance in adults vs children?

A

Laryngoscopy in adults = tachycardia and HTN
in infants = bradycardia and decreased CO

Hypoxia in adults = +/- tachycardia
in infants = bradycardia

102
Q

How to protect the HR in infants

A

use plenty of O2

103
Q

What is the effect of a high spinal in an adult vs an infant?

A

adult high spinal –> HoTN

infant high spinal –> no HoTN

104
Q

How does a patient with an immature thermoregulation system maintain heat?

A

brown fat (non-shivering thermogenesis)

Fun Fact: baby don’t shiver till they are 1 y/o

105
Q

3 reasons babies have greater heat loss than adults

A

Babies have

  • thin skin
  • low fat content
  • high surface area/wt ratio
106
Q

can babies be rewarmed easily?

A

YEP! =)

107
Q

At what point during gestation does urine flow begin?

A

10-12 weeks

108
Q

When during gestation is a baby’s renal function adequately developed for extra-uterine life?

A

mid gestation

109
Q

Compared to an adult, what is an infant’s ability to concentrate urine in the first year of life?

A

it is diminished in the first yr of life

110
Q

Why is meticulous attention to fluid admin especially important for an infant?

A

an infants renal function has a decreased EVERYTHING!!!

  • GFR
  • CrCl
  • Na excretion
  • glucose excretion
  • bicarb reabsorption
  • diluting capability
  • concentrating ability
111
Q

Infants in the first year of life have diminished urine concentrating ability compared to the adult. What is the main implication in light of this fact?

A

Babies have less capacity to compensate for fluid imbalances

112
Q

Preterm infant renal pathophys

name the things that are decreased plus the hormone that is out of balance

A
  • decreased GFR
  • decreased renal tubular Na threshold
  • decreased glucose threshold
  • decreased bicarb threshold
  • relative hypoaldosteronism –> increased risk of hyperK
113
Q

How does a child’s calories needed/day compare to the amt of fluid they need/day

A

number of kcal/kg/day should = mL/kg/day

Fun Fact: Metab of 1 Calorie of energy consumes 1 mL of H2O

114
Q

how to figure a child’s Maint IVF rate

A

4:2:1 rule (same as adults)

115
Q

Good options of MIVF for peds pts. Why?

A

D5LR
D5 1/2NS
D5 1/4NS
Kids burn through sugar much faster than adults

116
Q

difference in glucose mgmt between adults and peds

A

Peds have:

  1. high glucose utilization
  2. low glycogen stores
117
Q

hypoglycemia levels in neonates and infants (lab values)

A

neonates <30 mg/dl

infants <40 mg/dl

118
Q

Since pediatric pts have equal biventricular pressures, their stroke volume is fixed. What does this mean for the CO?

A

CO depends on HR

119
Q

Why do pediatric pts not become tachycardic in the case of hypovolemia/HoTN?

A

they have immature sympathetic and baroreceptor responses

120
Q

Name a serious dysrhythmia in a pediatric pt. What is usually its cause?

A

Bradycardia

Hypoxemia

121
Q

What are the differences between the circulation of an unborn baby, a neonate, and an adult?

A

unborn baby: pulm bed is high resistance. R side of the heart is decompressed: R-L flow at atrium and ductus

Neonate: SVR rises when the umbilical cord is clamped and PulmVR falls because of breathing and increased pO2 (L-R flow at atrium and ductus but fetal circulation is still possible)

Adult: R and L sides in series with no shunts

122
Q

What is persistent fetal circulation (PFC)?

A

Failure of the ductus to close

Fun Fact:
ductus usually closes at 12-15 hrs from muscular contraction

123
Q

4 factors that can reverse or prevent shunt closure –> PFC

A
  1. Hypoxemia
  2. Acidosis
  3. Critical medical/surgical illness
  4. structural heart dz
124
Q

What is the difference between the contractile elements of a newborn myocardium compared to an adult myocardium?

A

Contractile elements comprise 30% of newborn myocardium vs 60% of the adult myocardium

125
Q

What isoform of troponin predominates and what does this lead to?

A

Alpha isoform

More efficient binding therefore faster relaxation at increased HR

126
Q

Postnatal increase in myocardial mass is due to ______________

A

hypertrophy of existing myocytes

127
Q

How are the following characteristics of a neonatal heart different from an adult heart:

  1. CO
  2. Starling response
  3. Compliance
  4. Afterload compensation
  5. Ventricular interdependence
A
  1. CO HR dependent in NN (SV and HR dependent in adult)
  2. Starling response limited in NN
  3. Compliance less in NN
  4. Afterload compensation limited in NN
  5. Ventricular interdependence high in NN (relatively low in adults)
128
Q

What 3 hemodynamic principles apply to a baby?

A
  1. avoid (excessive) vasoconstriction
  2. maintain HR
  3. avoid rapid (excessive) fluid loading
129
Q

What drives CO in a pediatric pt?

A

Metab demand

130
Q

How s CO R/T Hgb in a pediatric pt?

A

it is inversely proportional

131
Q

Which hgb has a higher affinity for O2: Adult or fetal?

A

Fetal

[think about it. the fetal hgb has to pull O2 off from the mother’s Hgb]

132
Q

Equation to estimate allowable blood loss in infant

A

EABL = wt in kg x est blood vol x (starting Hct - allowable Hct) / Avg hct

133
Q

At what hit should premies and sick neonates be given blood?

A

Hct 40-50%

134
Q

Starting dose of PRBC, FFP, plt, and cryo for peds pt

A

PRBC: 10 mL/Kg
FFP: 10 mL/kg
Plt: 1 unit/10 kg (corresponds to a 50K increase in plts)
cryo: 1U/10 kg

135
Q

How does the myocute B-receptor density change from birth to postnatally?

A

Myocyte B-receptor density peaks at birth and declines postnatally, but the coupling mechanism is immature.

136
Q

At what point in gestation does a baby’s become tachycardic in response to isoproterenol and epi?

A

6 weeks gestation

137
Q

Formula to “guesstimate” a childs wt

A

2 x age + 9

138
Q

is the volume of distribution for water soluble meds going to be larger or smaller in a peds pt? why? what is the implication?

A

larger in a peds pt.

because total body water content is increased in a peds pt

increased dose/kg

139
Q

how are the following different in peds pts:

  1. hepatic biotransformation of meds
  2. protein binding
  3. NMJ
  4. Musc mass
A
  1. immature
  2. decreased at birth
  3. immature
  4. smaller therefore termination of action of a med by redistribution is prolonged
140
Q

Considerations of pediatric physiology that impact volatile anesthetics (4)

A
  1. minute ventilation to FRC ratio increased
  2. blood flow to vessel rich groups is increased (therefore they will have a rapid rise in alv anes concern)
  3. blood-gas coefficients are lower in neonates
  4. inhalation induction is rapid
141
Q

Why is inh induct of peds more rapid?

A

BP of neonates and infants are more sensitive to hemodynamic effects of IAs

Pediatric Physiology - B. Stevens/Bernstein 2017 (7 decks)

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