Transcript pedsPhysAirway

Pediatric Fundamentals
McGraw-Hill 2002
Pediatric Fundamentals
Objectives
Explain and apply to your anesthetic practice
selected elements of pediatric
Growth and development
Cardiovascular physiology
Respiratory physiology including
Airway maintenance
Pediatric Fundamentals – Prenatal Growth and Development
Prenatal
Embryonic period first 8 weeks
Organogenesis 4th – 8th weeks
Ectoderm
Mesoderm
Endoderm
Pediatric Fundamentals – Prenatal Growth and Development
Organogenesis 4th – 8th weeks
Mesoderm
somites
myotomes ->
segmental muscles of trunk
dermatomes ->
dermis of scalp, neck, trunk
sclerotomes ->
vertebral bodies, arches
abnormal induction -> spinal bifida
Pediatric Fundamentals – Prenatal Growth and Development
Developmental Abnormalities
congenital diaphragmatic hernia (CDH)
esophageal atresia
spina bifida
Hirschsprung’s disease
omphalocele
gastroschisis
Pediatric Fundamentals – Prenatal Developmental Abnormalities
Congenital diaphragmatic hernia (CDH)
1 in 2,500 live births
85% left side of diaphragm
defect in closure of pleuroperitoneal canal
impaired lung growth
prenatal (intrauterine) repair possible
Pediatric Fundamentals – Prenatal Developmental Abnormalities
Esophageal atresia
failure of proliferation of esophageal endoderm in 5th week
5 types – some with associated tracheoesophageal fistula
+ E = H-type
(7%)
10%
1%
80%
2%
Pediatric Fundamentals – Prenatal Developmental Abnormalities
Spina bifida
failure of closure of posterior neural tube during 3rd embryonic week
mild: spina bifida occulta
severe: meningomyelocele
80% lumbosacral
in utero repair described
Pediatric Fundamentals – Prenatal Developmental Abnormalities
Hirschsprung’s disease
defect in neural crest migration
leads to paralysis of that segment of colon
with subsequent proximal dilation
Pediatric Fundamentals – Prenatal Developmental Abnormalities
Omphalocele
1 in 2,500 live births
failure of return of midgut
from yolk sac to abdomen
by 10 weeks
often associated with other abnormalities
Pediatric Fundamentals – Prenatal Developmental Abnormalities
Gastroschisis
1 in 10,000 live births
abdominal wall defect
between developing rectus muscles
just lateral to umbilicus
right side
may be due to abnormal involution of right umbilical vein
during 5th and 6th weeks
usually not associated with other defects
Pediatric Fundamentals – Prenatal Growth and Development
Consequences of maternal disorders on intrauterine development
epilepsy
history of previous child with neural tube defect
diabetes mellitus
substance abuse
alcohol
tobacco
cocaine
benzodiazepines
infectious diseases
rubella
toxoplasmosis
human immunodeficiency virus (HIV)
herpes simplex
Pediatric Fundamentals –Consequences of Maternal Disorders
Epilepsy
Congenital anomalies 2 to 3 times more frequent
Appear to associated with increase risk of malformation:
phenytoin
valproic acid
multidrug therapy
Neural tube defects (e.g. spina bifida)
valproic acid
carbamazepine
low dose folate may decrease risk
Pediatric Fundamentals – Consequences of Maternal Disorders
History of previous neural tube defect:
Risk of subsequent neural tube defect
increased 10 times
Pediatric Fundamentals – Consequences of Maternal Disorders
Diabetes mellitus
Increased incidence of
stillbirth
congenital malformations
risk of major malformation
(8 times greater)
hypertophic cardiomyopathy in IDM
increased rate of high birth weight
Pediatric Fundamentals – Consequences of Maternal Disorders
Substance abuse
alcohol
Fetal alcohol syndrome
intrauterine growth retardation (IUGR)
microcephaly
characteristic facies
CNS abnormalities
with intellectual deficiency
Increased incidence of other major malformations
Pediatric Fundamentals – Consequences of Maternal Disorders
Tobacco
Cocaine
prematurity
clinical seizures
EEG abnormalities
neurobehavioral abnormalities
cerebral hermorrhagic infarction
Benzodiazepines:
no clear teratogenic link
sedation and/or withdrawal symptoms reported
Pediatric Fundamentals – Consequences of Maternal Disorders
Infectious disease
Rubella
Chromosomal abnormalities
IUGR
Ocular lesions
Deafness
Congenital cardiomyopathy
Especially with infections before week 11
Pediatric Fundamentals – Consequences of Maternal Disorders
Infectious disease
Toxoplasmosis
IUGR
Nonimmune hydrops
Hydrocephalus
Microcephaly
Later neurologic damage
Prompt spiramycin Rx until after delivery decreases risk 50%
Pediatric Fundamentals – Consequences of Maternal Disorders
Infectious disease
Human immunodeficiency virus (HIV)
Transmission to fetus: 12 – 30%
less if mother taking Zidovudine
(no teratogenesis reported)
First signs appear at 6 months of age
Median survival 38 months
Pediatric Fundamentals – Consequences of Maternal Disorders
Infectious disease
Herpes simplex
Neonatal infections
Two-thirds caused by asymptomatic genital infection
High morbidity and mortality
Seizures
Psychomotor retardation
Spasticity
Blindness
Learning disabilities
Death
Maternal active infection: C-section indicated to decrease risk
Pediatric Fundamentals – Consequences of Maternal Disorders
IUGR
3-7% of all pregnancies
Major cause of perinatal morbidity and mortallity
Prognosis depends on specific cause
Up to 8% have major malformations
Head growth important determinant of neurodevelopmental outcome
(IUGR + HC < 3rd%ile -> abnormal neurodevelopment likely)
Hemodynamic changes and/or infectious disease often involved
Pediatric Fundamentals - Prematurity
Definitions
premature: gestational age less than 37 weeks or 259 days
moderately premature: 31-36 weeks
severely premature: 24-30 weeks
postterm: greater than 41 weeks
low birth weight (LBW): < 2,500 Gm
(only a bit over half of LBW infants are premature)
very low birth weight (VLBW): < 1,500 Gm
newborn: first day of life
neonate: first month of life
infant: first year of life
Pediatric Fundamentals - Prematurity
5-10% of live births
High morbidity and mortality due to immature organ systems
Responsible for 75% of perinatal deaths
Immediate/early complications
hypoxia/ischemia
intraventricular hemorrhage
sensorineural injury
respiratory failure
necrotizing enterocolitis
cholestatic liver disease
nutrient deficiency
social stress
Pediatric Fundamentals - Prematurity
Special considerations
Respiratory
breathing may initially be exclusively nasal
spontaneous neck flexion may cause
airway obstruction and
apnea
diaphragm is most important respiratory muscle
fewer diaphragmatic type I fibers (10% vs 25%)
maternal betamethasone or dexamethasone
48 hours before delivery
increases surfactant production and
decreases mortality after 30 weeks gestation
Pediatric Fundamentals - Prematurity
Special considerations
Respiratory
apneas
25% of all prematures
alleviated with
caffeine or theophylline
PEEP
stimulation
may be exacerabated by general anesthesia
especially infants < 50 weeks postconceptional age
Pediatric Fundamentals - Prematurity
Special considerations
Cardiovascular
PDA - treatment
fluid restriction
diuretics
indomethacin
surgical ligation
Cardiac output relatively dependent on heart rate
Immature sympathetic innervation
Pediatric Fundamentals - Prematurity
Special considerations
Renal
urine flow begins 10-12 weeks gestation
decreased in premature (compared to full term)
GFR
renal tubular Na threshold
glucose threshold
bicarbonate threshold
relative hypoaldosteronism with
increased risk of hyperkalemia
tubular function develops significantly after 34 weeks
Pediatric Fundamentals - Prematurity
Special considerations
Nervous system
Brain has 2 growth spurts
1. neuronal cell multiplication 15-20 weeks gestation
2. glial cell multiplication 25 weeks to 2 years of life
Blood vessels more fragile
increased risk of intracerebral hemorrhage
Periventricular leukomalacia
ischemic cerebral complication
12-25% of LBW infants
increase risk of mental handicap
Retinopathy of prematurity
Pediatric Fundamentals - Prematurity
Special considerations
Thermal problems
Immature thermoregulation system
Body heat loss by
evaporation
conduction
convection
radiation
Pediatric Fundamentals - Growth and Development
Maturational change in form and function
Prenatal Growth
Gestational age (wks)
Mean birth wt (Gm)
25
850
28
1000
30
1400
33
1900
37
2900
40
3500
Postnatal Growth
Birth weight doubles by 5 months
triples by 1 year
Birth length doubles by 4 years
Pediatric Fundamentals - Growth and Development
Maturational change in form and function
Percent body water
Term newborn 80
1 year old
70
Adult
60
Surface area:Weight
premature > full term > infant > child
greater surface area
greater evaporative heat loss
rapid hypothermia if unprotected
Girls
Boys
Puberty onset
11 years
11½ years
Peak growth
Tanner stage 3
Tanner stage 4
Pediatric Fundamentals - Growth and Development
Fluid requirements
Metabolism of one calorie of energy consumes one ml of H2O,
so fluid requirements thought to reflect caloric requirement:
Body weight (kg)
Calories needed (kcal/kg/day) = Fluid requirement (ml/kg/day)
0-10
100
10-20
1000 + 50/(kg>10)
> 20
1500 + 20/(kg>20)
Dividing by 24 (hours/day) yields the famous
4:2:1 Rule for hourly maintenance fluid:
4 ml/kg/hr 1st 10 kg +
2 ml/kg/hr 2nd 10 kg +
1 ml/kg/hr for each kg > 20
Pediatric Fundamentals - Growth and Development
Airway/respiratory system
Gas exchange first possible approximately 24 weeks gestation
Surfactant production appears by approximately 27 weeks
produced of Type II pneumocytes
exogenous form available
Number (and size) of alveoli increase to age 8 years
(size only after 8 years)
First breaths of air
pneumothorax or pneumomediastinum less than 1%
several hours to reach normal lower lung fluid levels
some expelled during birth canal compression
transient tachypnea of newborn (TTN)
increased incidence after C-section
Pediatric Fundamentals - Growth and Development
Respiratory rate/rhythm
pauses up to 10 seconds normal in prematures
without cyanosis or bradycardia
Age (years)
Normal Rate
1-2
20 - 40
2-3
20 – 30
7-8
15 - 25
Obligate nose breathing
especially prematures
able to mouth breath if nares occluded
80% of term neonates
almost all term infants by 5 months
Pediatric Fundamentals - Growth and Development
Airway differences – infant vs adult
epiglottis and tongue relatively larger
glottis more superior, at level of C3 (vs C4 or 5)
cricoid ring narrower than vocal cord aperture
until approx 8 years of age
4.5 mm in term neonate
11 mm at 14 years
Pediatric Fundamentals - Growth and Development
Cardiovascular system
In utero circulation
placenta ->
umbilical vein (UV)->
ductus venosus (50%) ->
IVC ->
RA ->
foramen ovale (FO) ->
LA ->
Ascending Ao ->
SVC ->
RA ->
tricuspid valve ->
RV (2/3rds of CO) ->
main pulmonary artery (MPA) ->
ductus arteriosus (DA) (90%) ->
descending Ao ->
umbilical arteries (UAs)->
Pediatric Fundamentals - Growth and Development
Cardiovascular system
Transition to postnatal circulation
Loss of large low-resistance peripheral vascular bed, the placenta
(UV, UAs constrict over several days)
With first air breathing
marked drop in pulmonary vascular resistance with
greatly increased pulmonary blood flow
LA pressure > RA pressure
closes FO
Elevated PaO2 constricts DA
hours to days
Hgb F impairs postnatalO2 delivery
Higher newborn resting cardiac index
with decreased ability to further increase
Pediatric Fundamentals - Growth and Development
Cardiovascular system
Normal murmurs
up to 80% of normal children
vibratory Still’s murmur
basal systolic ejection murmur
physiologic peripheral pulmonic stenosis (PSS)
venous hum
carotid bruit
S3
Murmur only in diastole = abnormal
Pediatric Fundamentals - Growth and Development
Gastrointestinal notes
Gastric pH higher at birth; decreases over several weeks
Young infants
diminished lower esophageal sphincter tone
50% have daily emesis (usually remits by 18 months)
more show reflux if esophageal pH monitored
only 1 in 600 develop complications of reflux
Physiologic jaundice
Colic < 3 months
Umbilical hernia
common
frequently resolve spontaneously
Teeth
primary: 7 months to 2 or 3 years
permanent: 6 years to 20 years
Pediatric Fundamentals - Growth and Development
Renal system
Urine production begins first trimester
Newborn
GFR
low (correlates with gestational age/size in prematures)
rises sharply first 2 weeks
adult values by age 2 years
limited concentrating ability (600 vs adult 1200 mOsm/kg)
ability to dilute urine relatively intact
Pediatric Fundamentals - Growth and Development
Hematologic system
Infant Hgb F – higher O2 affinity
Hgb A production largely replaces Hgb F by 4 months
Hgb/Hct decrease to nadir at about age 2 months
exaggerated in prematures (low total body Fe stores)
Blood volume (ml/kg)
Prematures
105
Term newborn
85
Adult
65
Pediatric Fundamentals - Growth and Development
Neuro notes
Nervous system anatomically complete at birth
except:
Myelination
rapid for 2 years
complete by 7 years
Posterior fontanelle closed by 6 weeks
Anterior fontanelle closed by 18 months
Primitive reflexes disappear in few months
Pediatric Fundamentals - Growth and Development
Developmental pediatrics
Approach to patient depends on stage of development
Stranger anxiety
7 months
25%
9
50
12
75
Toddlers
magical thinking (belief that own thought or deed causes external events)
temper tantrums (aggravated if tired, ill, uncomfortable)
Toilet training
ability develops by 18 months
usually complete by 2 to 3 years (day before night)
bedwetting
15 - 20 % at 5 years with gradual decrease to
1% at 15 years
6 -11 years - concrete operations phase
can consider different points of view
develop explanation based on observation
beginning logical reasoning but still tend to dogmatic
11 and older - development of abstract thinking
Adolescent - increasing need for autonomy, participation in care
http://metrohealthanesthesia.com/edu/ped/pedspreop3.htm
Pediatric Fundamentals - Growth and Development
Developmental pediatrics
History and physical notes
Newborn – pregnancy and delivery
Infancy – developmental milestones
Toddler – poor localization of symptoms and very suggestible
(e.g., pharyngitis or pneumonia presenting as
abdominal pain or distress)
Older child – involve in discussion/decision
Preadolescent and older – consider interview without parents
Exam
opportunistic approach in infants and young children
observation essential
distraction useful
Pediatric Fundamentals – Heart and Circulation
Embryology
1. Cardiovascular system begins forming at 3 weeks
(diffusion no longer adequate)
2. Angiogenetic cell cluster and blood islands ->
intraamniotic blood vessels
3. Heart tube
4. Heart begins to beat 22 – 23 days
5. Heart looping -> 4 chambers, 27 – 37 days
6. Valves 6 – 9 weeks
Pediatric Fundamentals – Heart and Circulation
Transitional circulation
Placenta Out and Lungs In
PVR drops dramatically
(endothelial-derived NO and prostacyclin)
FO closes
DA closes
10-12 hours to 3 days to few weeks
prematures: closes in 4-12 months
PFO potential route for systemic emboli
DA and PFO routes for R -> L shunt in PPHN
Pediatric Fundamentals – Heart and Circulation
Persistent pulmonary hypertension of the newborn (PPHN)
Old PFC misnomer
Primary
Secondary
meconium aspiration
sepsis
birth asphyxia
Treatment
cardiopulmonary support
inhaled NO
ECMO
Pediatric Fundamentals – Heart and Circulation
Nitric oxide (NO) – cGMP transduction pathway
l-arginine
↓
eNOS (endothelial NO synthetase)
oxidation of quanidine N moiety
NO
activates
↓
GTP
↓
sGC (soluble guanylate cyclase)
cGMP (cyclic-3’,5’-guanosine monophosphate)
activates
↓
protein kinase
PDE (phosphodiesterase)
GMP
Pediatric Fundamentals – Heart and Circulation
Neonatal myocardial function
Contractile elements comprise 30% (vs 60% adult) of newborn myocardium
Alpha isoform of tropomyosin predominates
more efficient binding for faster relaxation at faster heart rates
Relatively disorganized myocytes and myofibrils
Most of postnatal increase in myocardial mass due to
hypertrophy of existing myocytes
Diminished role of relatively disorganized sarcomplasmic reticulum (SR)
and greater role of Na-Ca channels in Ca flux so
greater dependence on extracellular Ca
may explain:
Increased sensitivity to
calcium channel blockers (e.g. verapamil)
hypocalcemia
digitalis
Pediatric Fundamentals – Heart and Circulation
Myocardial energy metabolism
Young infant heart
lactate: primary metabolite
later: glucose oxidation and amino acids (aa’s)
metabolize glucose and aa’s under hypoxic conditions
(may lead to greater tolerance of ischemic insults)
Gradual transition to adult:
fatty acid primary metabolite by 1-2 years
Pediatric Fundamentals – Heart and Circulation
Normal aortic pressures
Wt (Gm)
1000
2000
3000
4000
Age (months)
1
3
6
9
12
Sys/Dias
50/25
55/30
60/35
70/40
mean
35
40
50
50
Sys/Dias mean
85/65
50
90/65
50
90/65
50
90/65
55
90/65
55
Pediatric Fundamentals – Heart and Circulation
Adrenergic receptors
Sympathetic receptor system
Tachycardic response to isoproterenol and epinephrine
by 6 weeks gestation
Myocyte β-adrenergic receptor density
peaks at birth then
decreases postnatally
but coupling mechanism is immature
Parasympathetic, vagally-mediated responses are mature at birth
(e.g. to hypoxia)
Babies are vagotonic
Pediatric Fundamentals – Heart and Circulation
Normal heart rate
Age (days)
1-3
4-7
8-15
Rate
100-140
80-145
110-165
Age (months) Rate
0-1
100-180
1-3
110-180
3-12
100-180
Age (years)
1-3
3-5
5-9
9-12
12-16
Rate
100-180
60-150
60-130
50-110
50-100
Pediatric Fundamentals – Heart and Circulation
Newborn myocardial physiology
Type I collagen (relatively rigid) predominates (vs type III in adult)
Cardiac output
Starling response
Compliance
Afterload compensation
Ventricular
interdependence
Neonate
HR dependent
limited
less
limited
high
Adult
SV & HR dependent
normal
normal
effective
relatively low
So:
Avoid (excessive) vasoconstriction
Maintain heart rate
Avoid rapid (excessive) fluid administration
Pediatric Respiratory Physiology
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
Mesenchymal elements develop into
smooth muscle
cartilage
connective tissue
vessels
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
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 ->
IRDS (HMD) due to insufficient surfactant production
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
Pediatric Respiratory Physiology
Prenatal Development
Lung Fluid
expands airways -> helps stimulate lung growth
contributes ⅓ of total amniotic fluid
prenatal ligation of trachea in congenital diaphragmatic hernia
results in accelerated growth of otherwise hypoplastic lung
(J Pediatr Surg 28:1411, 1993)
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 ->
increased left atrial pressure with
closure of foramen ovale
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
Pediatric Respiratory Physiology
Infant lung volume disproportionately small in relation to body size
VO2/kg = 2 x adult value
=> ventilatory requirement per unit lung volume is increased
less reserve
more rapid drop in SpO2 with hypoventilation
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
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
Pediatric Respiratory Physiology
Control of breathing – prenatal development
fetal breathing
during REM sleep
depressed by hypoxia
(severe hypoxia -> gasping)
may enhance lung growth and development
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
Independent of PaCO2; unaffected by carotid denervation
Hypoxia depresses or abolishes coninuous breathing
Pediatric Respiratory Physiology
Control of breathing – infants
Ventilatory response to hypoxemia
first weeks (neonates)
transient increase -> 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)
Pediatric Respiratory Physiology
Periodic breathing
apneic spells < 10 seconds
without cyanosis or bradycardia
(mostly 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
Pediatric Respiratory Physiology
Central apnea
apnea > 15 seconds or
briefer but associated with
bradycardia (HR<100)
cyanosis or
pallor
rare in full term
majority of prematures
Pediatric Respiratory Physiology
Postop apnea in preterms
Preterms < 44 weeks postconceptional age (PCA): risk of apnea = 20-40%
most within 12 hours postop (Liu, 1983)
Postop apnea 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 < 5% (Cote, 1995)
Except: Hct < 30: risk remains HIGH independent of PCA
Role for caffeine (10 mg/kg IV) in prevention of postop apnea in prematures?
(Wellborn, 1988)
Pediatric Respiratory Physiology – Pulmonary and Thoracic Receptors
Upper airway
Pharyngeal receptors ->
inhibition of breathing
closure of larynx
contraction of pharyngeal swallowing muscles
Pediatric Respiratory Physiology – Pulmonary and Thoracic Receptors
Upper airway - Larynx
three receptor types
pressure
drive (irritant)
flow (or cold)
response to stimulus
apnea
coughing
closure of glottis
laryngospasm
changes in ventilatory pattern
newborn
increased sensitivity to superior laryngeal nerve stimulus ->
ventilatory depression or apnea
H2O more potent stimulus than normal saline ([Cl-])
Pediatric Respiratory Physiology – Pulmonary and Thoracic Receptors
Infant (especially preterm) reflex response to fluid at entrance to larynx
Normal protective
swallowing
central apnea (H2O > NS)
sneezing
laryngeal closure
coughing or awakening (less frequent)
During inhalation induction
pharyngeal swallowing reflex abolished
laryngeal reflex intact ->
breath holding or central apnea
positive pressure ventilation may ->
push secretions into larynx ->
laryngospasm
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 < 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
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
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 ->
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
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
hypersecretion
hypotension
bradycardia
maybe laryngospasm
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
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 ->
C.N. IX, glossopharyngeal nerve
Stimulus
paCO2 and pH
paO2 (especially < 60 mmHg)
Response – increased ventilation
Contribute 15% of resting ventilatory drive
Neonate: hypoxia depresses ventilation
by direct suppression of medullary centers
Pediatric Respiratory Physiology – Chemical Control of Breathing
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)
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 ->
hypoventilation with
markedly elevated paCO2
Pediatric Respiratory Physiology – Assessment of Respiratory Control
CO2 response curve
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 ->
upper airway obstruction (infants > adults)
work of breathing decreased with
jaw lift
CPAP 5 cmH2O
oropharyngeal airway
LMA
Active expiration (halothane)
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
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
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 < closing capacity leading to
small airway closure
atalectasis
V/Q mismatch
declining SpO2
Pediatric Respiratory Physiology – Lung Volumes and Mechanics of Breathing
General anesthesia, FRC and PEEP
Mean PEEP to resore FRC to normal
infants < 6 months 6 cm H2O
children
6-12 cm H2O
PEEP
important in children < 3 years
essential in infants < 9 months
under GA + muscle relaxants
(increases total compliance by 75%)
(Motoyama)
Pediatric Respiratory Physiology – Dynamic Properties
Poiseuille’s law for laminar flow:
where
R = 8lη/πr4
For turbulent flow:
R resistance
l length
η viscosity
R α 1/r5
Upper airway resistance
adults: nasal passages: 65% of total resistance
Infants: nasal resistance 30-50% of total
upper airway: ⅔ of total resistance
NG tube increases total resistance up to 50%
Pediatric Respiratory Physiology
Anesthetic effects on respiratory mechanics
Relaxation of respiratory muscles ->
decreased FRC
cephalad displacement of diaphragm
contributes 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
Pediatric Respiratory Physiology
Anesthetic effects on respiratory mechanics
Endotracheal tube adds the most significant resistance
Pediatric Respiratory Physiology
Ventilation and pulmonary circulation
Infants: VA per unit of lung volume > 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
Pediatric Respiratory Physiology
Oxygen transport
(Bohr effect)
= 27, normal adult (19, fetus/newborn)
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
9 months
P50 = 27 (adult level)
P50 peaks at 29-30
Pediatric Respiratory Physiology
Oxygen transport
If SpO2 = 91
then = PaO2 =
Adult
6 months
6 weeks
6 hours
60
66
55
41
Pediatric Respiratory Physiology
P50
Oxygen transport
Hgb for equivalent tissue oxygen delivery
Adult
27
8
10
12
> 3 months
30
6.5
8.2
9.8
< 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
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
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
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)
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
More Pediatric Airway Info at
MetroHealthAnesthesia.com