Pediatric Respiratory Physiology

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Pediatric Respiratory Physiology
Drs. Greg and Joy Loy Gordon February 2005
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Pediatric Respiratory Physiology
Prenatal Embryo
Ventral pouch in primitive foregut becomes lung
buds projecting into pleuroperitoneal
cavity Endodermal part develops
into airway alveolar membranes glands Mesenchym
al elements develop into smooth
muscle cartilage connective tissue vessels
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Pediatric Respiratory Physiology
Prenatal Development
Pseudoglandular period starting 17th week of
gestation Branching of airways down to terminal
bronchioles Canalicular period Branching in to
future respiratory bronchioles Increased
secretary gland and capillary formation Terminal
sac (alveolar) period 24th week of
gestation Clusters of terminal air sacs with
flattened epithelia
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Pediatric Respiratory Physiology
Surfactant
Produced by type II pneumocytes appear 24-26
weeks (as early as 20 weeks) Maternal
glucocorticoid treatment 24-48 hours before
delivery accelerates lung maturation and
surfactant production Premature birth
immature lungs -gt IRDS (HMD) due to
insufficient surfactant production
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Pediatric Respiratory Physiology
Prenatal Development
Proliferation of capillaries around saccules
sufficient for gas exchange 26-28th week (as
early as 24th week) Formation of alveoli 32-36
weeks saccules still predominate at birth
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Pediatric Respiratory Physiology
Prenatal Development
Lung Fluid expands airways -gt helps stimulate
lung growth contributes ? of total amniotic
fluid prenatal ligation of trachea in congenital
diaphragmatic hernia results in accelerated
growth of otherwise hypoplastic lung (J
Pediatr Surg 281411, 1993)
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Pediatric Respiratory Physiology
Perinatal adaptation
First breath(s) up to 40 (to 80 cmH2O needed
to overcome high surface forces to introduce
air into liquid-filled lungs adequate surfactant
essential for smooth transition Elevated PaO2
Markedly increased pulmonary blood flow
-gt increased left atrial pressure with closure
of foramen ovale
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Pediatric Respiratory Physiology
Postnatal development
Lung development continues for 10 years most
rapidly during first year At birth 20-50x107
terminal air sacs (mostly saccules) only one
tenth of adult number Development of alveoli from
saccules essentially complete by 18 months of
age
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Pediatric Respiratory Physiology
Infant lung volume disproportionately small in
relation to body size VO2/kg 2 x adult value
gt ventilatory requirement per unit lung volume
is increased less reserve more rapid drop in
SpO2 with hypoventilation
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Pediatric Respiratory Physiology
Neonate Lung compliance high elastic fiber
development occurs postnatally static elastic
recoil pressure is low Chest wall compliance is
high cartilaginous ribs limited thoracic muscle
mass More prone to atalectasis and respiratory
insufficiency especially under general
anesthesia Infancy and childhood static recoil
pressure steadily increases compliance,
normalized for size, decreases
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Pediatric Respiratory Physiology
Infant and toddler more prone to severe
obstruction of upper and lower airways absolute
airway diameter much smaller that
adult relatively mild inflammation, edema,
secretions lead to greater degrees of
obstruction
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Pediatric Respiratory Physiology
Control of breathing prenatal
development fetal breathing during REM
sleep depressed by hypoxia (severe hypoxia
-gt gasping) may enhance lung growth and
development
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Pediatric Respiratory Physiology
Control of breathing perinatal adaptation
Neonatal breathing is a continuation of fetal
breathing Clamping umbilical cord is important
stimulus to rhythmic breathing Relative hyperoxia
of air augments and maintains rhythmicity Independ
ent of PaCO2 unaffected by carotid
denervation Hypoxia depresses or abolishes
coninuous breathing
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Pediatric Respiratory Physiology
Control of breathing infants Ventilatory
response to hypoxemia first weeks
(neonates) transient increase -gt sustained
decrease (cold abolishes the transient increase
in 32-37 week premaures by 3 weeks sustained
increase
Ventilatory response to CO2 slope of
CO2-response curve decreases in
prematures increases with postnatal
age neonates hypoxia shifts CO2-response
curve and decreases slope (opposite to adult
response)
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Pediatric Respiratory Physiology
Periodic breathing apneic spells lt 10
seconds without cyanosis or bradycardia (mostl
y during quiet sleep) 80 of term neonates
100 of preterms 30 of infants 10-12 months
of age may be abolished by adding 3 CO2 to
inspired gas
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Pediatric Respiratory Physiology
Central apnea apnea gt 15 seconds or briefer
but associated with bradycardia
(HRlt100) cyanosis or pallor rare in full
term majority of prematures
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Pediatric Respiratory Physiology
Postop apnea in preterms
Preterms lt 44 weeks postconceptional age (PCA)
risk of apnea 20-40 most within 12 hours
postop (Liu, 1983)
Postop apnea reported in reported in prematures
as old as 56 weeks PCA (Kurth,
1987)
Associated factors extent of surgery anesthesia
technique anemia postop hypoxia (Wellborn,
1991)
44-60 weeks PCA risk of postop apnea lt 5 (Cote,
1995) Except Hct lt 30 risk remains HIGH
independent of PCA
Role for caffeine (10 mg/kg IV) in prevention of
postop apnea in prematures?
(Wellborn, 1988)
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Pediatric Respiratory Physiology Pulmonary and
Thoracic Receptors
Upper airway Pharyngeal receptors -gt inhibition
of breathing closure of larynx contraction of
pharyngeal swallowing muscles
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Pediatric Respiratory Physiology Pulmonary and
Thoracic Receptors
Upper airway - Larynx three receptor
types pressure drive (irritant) flow (or
cold) response to stimulus apnea coughing c
losure of glottis laryngospasm changes in
ventilatory pattern newborn increased
sensitivity to superior laryngeal nerve stimulus
-gt ventilatory depression or apnea H2O more
potent stimulus than normal saline (Cl-)
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Pediatric Respiratory Physiology Pulmonary and
Thoracic Receptors
Infant (especially preterm) reflex response to
fluid at entrance to larynx
Normal protective swallowing central apnea (H2O
gt NS) sneezing laryngeal closure coughing or
awakening (less frequent)
During inhalation induction pharyngeal
swallowing reflex abolished laryngeal reflex
intact -gt breath holding or central
apnea positive pressure ventilation may -gt
push secretions into larynx -gt laryngospasm
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Pediatric Respiratory Physiology Pulmonary and
Thoracic Receptors
Laryngospasm
Sustained tight closure of vocal cords by
contraction of adductor (cricothyroid)
muscles persisting after removal of initial
stimulus More likely (decreased threshold)
with light anesthesia hyperventilation with
hypocapnia Less likely (increased threshold)
with hypoventilation with hypercapnia positive
intrathoracic pressure deep anesthesia maybe
positive upper airway pressure Hypoxia (paO2 lt
50) increases threshold (fail-safe mechanism?)
So suction before extubation while patient
relatively deep and inflate lungs and maybe a
bit of PEEP at time of extubation
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Pediatric Respiratory Physiology Pulmonary and
Thoracic Receptors
Slowly adapting (pulmonary stretch) receptors
(SARs)
Posterior wall of trachea and major
bronchi Stimulus distension of airway during
inspiration hypocapnia Response inhibit
inspiratory activity (Hering-Breuer inflation
reflex) May be related to adult apnea with ETT
cuff inflated during emergence from anesthesia
and rhythmic breathing promptly on cuff
deflation
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Pediatric Respiratory Physiology Pulmonary and
Thoracic Receptors
Rapidly adapting (irritant) receptors (RARs)
Especially carina and large bronchi Stimulus lung
distortion smoke inhaled anesthetics histamine
Response coughing bronchospasm tracheal mucus
secretion Likely mediate the paradoxical reflex
of Head with vagal afferents partially blocked
by cold, inflation of lungs -gt sustained
contraction of diaphragm with prolonged
inflation may be related to sigh mechanism
(triggered by collapse of parts of lung
during quiet breathing and increasing surface
force) neonatal response to mechanical lung
inflation with deep gasping breath
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Pediatric Respiratory Physiology Pulmonary and
Thoracic Receptors
C-fiber endings (J-receptors)
Juxta-pulmonary receptors Stimulus pulmonary
congestion edema micro-emboli inhaled
anesthetic agents Response apnea followed by
rapid, shallow breathing bronchospasm hypersec
retion hypotension bradycardia maybe
laryngospasm
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Pediatric Respiratory Physiology Chemical
Control of Breathing
Central Chemoreceptors
Near surface of ventrolateral medulla Stimulus H
(pH of CSF and interstitial fluid
readily altered by changes in
paCO2) Response increased ventilation,
hyperventilation
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Pediatric Respiratory Physiology Chemical
Control of Breathing
Peripheral Chemoreceptors
Carotid bodies 3 types of neural
components type I (glomus) cells type II
(sheath) cells sensory nerve fiber
endings carotid nerve -gt C.N. IX,
glossopharyngeal nerve Stimulus paCO2 and
pH paO2 (especially lt 60 mmHg) Response
increased ventilation Contribute 15 of resting
ventilatory drive Neonate hypoxia depresses
ventilation by direct suppression of medullary
centers
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Pediatric Respiratory Physiology Chemical
Control of Breathing
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Pediatric Respiratory Physiology Chemical
Control of Breathing
Chronic hypoxemia (for years)
Carotid bodies lose hypoxemic response E.g.,
cyanotic congenital heart disease (but hypoxic
response does return after correction and
restoration of normoxia)
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Pediatric Respiratory Physiology Chemical
Control of Breathing
Chronic respiratory insufficiency with hypercarbia
Hypoxemic stimulus of carotid chemoreceptors
becomes primary stimulus of respiratory
centers Administration of oxygen may
-gt hypoventilation with markedly elevated
paCO2
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Pediatric Respiratory Physiology Assessment of
Respiratory Control
CO2 response curve
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Pediatric Respiratory Physiology Assessment of
Respiratory Control
Effects of anesthesia on respiratory control
Shift CO2 response curve to right Depress
genioglossus, geniohyoid, other phayrngeal
dilator muscles -gt upper airway obstruction
(infants gt adults) work of breathing decreased
with jaw lift CPAP 5 cmH2O oropharyngeal
airway LMA Active expiration (halothane)
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Pediatric Respiratory Physiology Lung Volumes
and Mechanics of Breathing
60 ml/kg infant
after 18 months increases to adult 90 ml/kg by
age 5
50 of TLC

may be only 15 of TLC in young infants under
GA plus muscle relaxants
25 TLC
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Pediatric Respiratory Physiology Lung Volumes
and Mechanics of Breathing
Elastic properties, compliance and FRC
Neonate chest wall compliance, CW 3-6 x CL,
lung compliance tending to decrease FRC,
functional residual capacity By 9-12 months CW
CL
Dynamic FRC in awake, spontaneously ventilating
infants is maintained near values seen in older
children and adults because of 1. continued
diaphragmatic activity in early expiratory
phase 2. intrinsic PEEP (relative tachypnea with
start of inspiration before end of preceding
expiration) 3. sustained tonic activity of
inspiratory muscles (probably most
important) By 1 year of age, relaxed
end-expiratory volume predominates
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Pediatric Respiratory Physiology Lung Volumes
and Mechanics of Breathing
Under general anesthesia, FRC declines by
10-25 in healthy adults with or without muscle
relaxants and 35-45 in 6 to 18 year-olds
In young infants under general anesthesia
especially with muscle relaxants FRC may
only 0.1 - 0.15 TLC FRC may be lt closing
capacity leading to small airway
closure atalectasis V/Q mismatch declinin
g SpO2
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Pediatric Respiratory Physiology Lung Volumes
and Mechanics of Breathing
General anesthesia, FRC and PEEP
Mean PEEP to resore FRC to normal infants lt 6
months 6 cm H2O children 6-12 cm H2O
PEEP important in children lt 3 years essential
in infants lt 9 months under GA muscle
relaxants (increases total compliance by
75) (Motoyama)
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Pediatric Respiratory Physiology Dynamic
Properties
Poiseuilles law for laminar flow
where R resistance l length ? viscosity
R 8l?/pr4
For turbulent flow R a 1/r5
Upper airway resistance adults nasal passages
65 of total resistance Infants nasal
resistance 30-50 of total upper airway ? of
total resistance NG tube increases total
resistance up to 50
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Pediatric Respiratory Physiology
Anesthetic effects on respiratory mechanics
Relaxation of respiratory muscles -gt decreased
FRC cephalad displacement of diaphragm contribu
tes to decreased FRC much less if patient not
paralyzed airway closure atalectasis minimized
by PEEP 5 cm H2O in children process slowed by
30-40 O2 in N2 (vs 100 O2) V/Q
mismatch Endotracheal tube adds the most
significant resistance
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Pediatric Respiratory Physiology
Ventilation and pulmonary circulation
Infants VA per unit of lung volume gt adult
because of relatively higher metabolic rate,
VO2 relatively smaller lung volume
Infants and toddlers to age 2 years VT
preferentially distributed to uppermost part of
lung
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Pediatric Respiratory Physiology
Oxygen transport
(Bohr effect)
27, normal adult (19, fetus/newborn)
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Pediatric Respiratory Physiology
Oxygen transport
Bohr effect increasing pH (alkalosis) decreases
P50 beware hyperventilation decreases tissue
oxygen delivery
Hgb F reacts poorly with 2.3-DPG P50 19
By age 3 months P50 27 (adult level) 9
months P50 peaks at 29-30
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Pediatric Respiratory Physiology
Oxygen transport
If SpO2 91 then PaO2
Adult 60 6 months 66 6 weeks 55 6
hours 41
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Pediatric Respiratory Physiology
Oxygen transport
P50 Hgb for equivalent tissue oxygen
delivery Adult 27 8 10 12 gt 3 months 30
6.5 8.2 9.8 lt 2 months 24 11.7 14.7 17.6
Implications for blood transfusion older infants
may tolerate somewhat lower Hgb levels at
which neonates ought certainly be transfused
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Pediatric Respiratory Physiology
Surfactant
Essential phospholipid protein complex Regulates
surface tension Stabilizing alveolar pressure
LaPlace equation P nT/r where P ressure r
adius of small sphere T ension n 2 for
alveolus
Surface tension 65 of elastic recoil pressure
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Pediatric Respiratory Physiology
Surfactant
Produced by cuboidal type II alveolar pneumocytes
(27th week) Lecithin (phosphatidylcholine,
PC)/sphingomyelin (L/S) ratio in amniotic fluid
correlates with lung maturity
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Pediatric Respiratory Physiology
Surfactant
Synthesis increased by glucocorticoids thyroxine
heroin cyclic adenosine monophosphate
(cAMP) epidermal growth factor tumor necrosis
factor alpha transforming growth factor beta
Synthetic surfactant used in treatment
of premature infants with surfactant deficiency
PPHN CDH meconium aspiration syndrome ARDS
(adults and children)
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Pediatric Respiratory Physiology Selected Points
Basic postnatal adaptation lasts until 44 weeks
postconception, especially in terms of
respiratory control Postanesthetic apnea is
likely in prematures, especially anemic Formation
of alveoli essentially complete by 18 months Lung
elastic and collagen fiber development continues
through age 10 years Young infant chest wall is
very compliant and incapable of sustaining FRC
against lung elastic recoil when under general
anesthesia, especially with muscle
relaxants leading to airway closure and
progressive atalectasis of anesthesia Mild
moderate PEEP (5 cmH2O) alleviates Hemoglobin
oxygen affinity changes dramatically first months
of life Hgb F low P50 (19) P50 increases,
peaks in later infancy (30) implications for
blood transfusion