pediatric fundamentals. mcgraw-hill 2002 pediatric fundamentals objectives growth and development...

Pediatric Fundamentals

McGraw-Hill 2002

Pediatric Fundamentals

Objectives

Growth and development

Cardiovascular physiology

Respiratory physiology including

Airway maintenance

Explain and apply to your anesthetic practice selected elements of pediatric

Pediatric Fundamentals – Prenatal Growth and Development

Prenatal

Embryonic period first 8 weeks

Organogenesis 4th – 8th weeks

Ectoderm

Mesoderm

Endoderm


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


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


Esophageal atresia

failure of proliferation of esophageal endoderm in 5th week

5 types – some with associated tracheoesophageal fistula

+ E = H-type(7%)

80%10%1% 2%


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


Hirschsprung’s disease

defect in neural crest migration

leads to paralysis of that segment of colonwith subsequent proximal dilation



failure of return of midgut

from yolk sac to abdomen

by 10 weeks

often associated with other abnormalities

Omphalocele



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

Gastroschisis


Consequences of maternal disorders on intrauterine developmentepilepsyhistory of previous child with neural tube defectdiabetes mellitussubstance abuse

alcoholtobacco cocainebenzodiazepines

infectious diseasesrubellatoxoplasmosishuman 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


Diabetes mellitus

Increased incidence of

stillbirth

congenital malformations

risk of major malformation

(8 times greater)

increased rate of high birth weight

hypertophic cardiomyopathy in IDM


Substance abuse

alcoholFetal alcohol syndrome

intrauterine growth retardation (IUGR)

microcephaly

characteristic facies

CNS abnormalities

with intellectual deficiency

Increased incidence of other major malformations


Tobacco Low birth weight

Cocaineprematurity

clinical seizures

EEG abnormalities

neurobehavioral abnormalities

cerebral hermorrhagic infarction

Benzodiazepines: no clear teratogenic link sedation and/or withdrawal symptoms reported


Infectious disease

Rubella

Chromosomal abnormalities

IUGR

Ocular lesions

Deafness

Congenital cardiomyopathy

Especially with infections before week 11


Infectious disease

Toxoplasmosis

IUGR

Nonimmune hydrops

Hydrocephalus

Microcephaly

Later neurologic damage

Prompt spiramycin Rx until after delivery decreases risk 50%


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


Infectious disease

Herpes simplex

Neonatal infectionsTwo-thirds caused by asymptomatic genital infectionHigh morbidity and mortality

Seizures Psychomotor retardation Spasticity Blindness Learning disabilities Death

Maternal active infection: C-section indicated to decrease risk


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


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 - PrematuritySpecial 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


apneas

25% of all prematures

alleviated with

caffeine or theophylline

PEEP

stimulation

may be exacerabated by general anesthesia

especially infants < 50 weeks postconceptional age

Respiratory

Special considerations

Pediatric Fundamentals - PrematuritySpecial considerations

Cardiovascular

PDA - treatment

fluid restriction

diuretics

indomethacin

surgical ligation

Cardiac output relatively dependent on heart rate

Immature sympathetic innervation

http://metrohealthanesthesia.com/edu/ped/chd6.htm#PDALigation



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



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



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 GrowthGestational age (wks) Mean birth wt (Gm)

25 85028 100030 140033 190037 290040 3500

Postnatal GrowthBirth weight doubles by 5 months

triples by 1 yearBirth length doubles by 4 years


Maturational change in form and function

Percent body waterTerm newborn 801 year old 70Adult 60

Surface area:Weightpremature > full term > infant > childgreater surface area

greater evaporative heat lossrapid hypothermia if unprotected

Girls Boys

Puberty onset 11 years 11½ years

Peak growth Tanner stage 3 Tanner stage 4


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

Fluid requirements


Airway/respiratory system

Gas exchange first possible approximately 24 weeks gestationSurfactant production appears by approximately 27 weeks

produced of Type II pneumocytesexogenous form available

Number (and size) of alveoli increase to age 8 years(size only after 8 years)

First breaths of airpneumothorax or pneumomediastinum less than 1%several hours to reach normal lower lung fluid levels

some expelled during birth canal compressiontransient tachypnea of newborn (TTN)

increased incidence after C-section


Respiratory rate/rhythmpauses up to 10 seconds normal in prematures

without cyanosis or bradycardiaAge (years) Normal Rate1 - 2 20 - 402 - 3 20 – 307 - 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


Airway differences – infant vs adultepiglottis and tongue relatively largerglottis 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 neonate11 mm at 14 years


Cardiovascular system

In utero circulationplacenta ->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)->


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



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


Gastrointestinal notes

Gastric pH higher at birth; decreases over several weeksYoung infants

diminished lower esophageal sphincter tone50% have daily emesis (usually remits by 18 months)more show reflux if esophageal pH monitoredonly 1 in 600 develop complications of reflux

Physiologic jaundiceColic < 3 monthsUmbilical hernia

commonfrequently resolve spontaneously

Teethprimary: 7 months to 2 or 3 yearspermanent: 6 years to 20 years


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


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


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


Developmental pediatrics

Approach to patient depends on stage of developmentStranger anxiety 7 months 25%

9 50 12 75

Toddlersmagical thinking (belief that own thought or deed causes external events)temper tantrums (aggravated if tired, ill, uncomfortable)

Toilet trainingability develops by 18 monthsusually 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 phasecan consider different points of viewdevelop explanation based on observationbeginning logical reasoning but still tend to dogmatic

11 and older - development of abstract thinkingAdolescent - increasing need for autonomy, participation in carehttp://metrohealthanesthesia.com/edu/ped/pedspreop3.htm

http://metrohealthanesthesia.com/edu/ped/pedspreop3.htm


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


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


Persistent pulmonary hypertension of the newborn (PPHN)

Old PFC misnomer

Primary

Secondary

meconium aspiration

sepsis

birth asphyxia

Treatment

cardiopulmonary support

inhaled NO

ECMO


Nitric oxide (NO) – cGMP transduction pathway

l-arginine

eNOS (endothelial NO synthetase)↓NO

oxidation of quanidine N moiety

sGC (soluble guanylate cyclase)

↓activates

↓GTP

cGMP (cyclic-3’,5’-guanosine monophosphate)activates

↓protein kinase

↓GMP

PDE (phosphodiesterase)


Neonatal myocardial function

Contractile elements comprise 30% (vs 60% adult) of newborn myocardiumAlpha isoform of tropomyosin predominates

more efficient binding for faster relaxation at faster heart ratesRelatively disorganized myocytes and myofibrilsMost of postnatal increase in myocardial mass due to

hypertrophy of existing myocytesDiminished role of relatively disorganized sarcomplasmic reticulum (SR)

and greater role of Na-Ca channels in Ca flux sogreater dependence on extracellular Camay explain:

Increased sensitivity to calcium channel blockers (e.g. verapamil)hypocalcemiadigitalis


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


Normal aortic pressures

Wt (Gm) Sys/Dias mean1000 50/25 352000 55/30 403000 60/35 504000 70/40 50

Age (months) Sys/Dias mean 1 85/65 50 3 90/65 50 6 90/65 50 9 90/65 55 12 90/65 55


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


Normal heart rate

Age (days) Rate 1-3 100-140 4-7 80-145 8-15 110-165

Age (months) Rate 0-1 100-180 1-3 110-180 3-12 100-180

Age (years) Rate 1-3 100-180 3-5 60-150 5-9 60-130 9-12 50-11012-16 50-100


Newborn myocardial physiology

Type I collagen (relatively rigid) predominates (vs type III in adult)

Neonate AdultCardiac output HR dependent SV & HR dependentStarling response limited normalCompliance less normalAfterload compensation limited effectiveVentricular high relatively low interdependence

So:

Avoid (excessive) vasoconstrictionMaintain heart rateAvoid rapid (excessive) fluid administration

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


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

Prenatal Development


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


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



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)



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


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


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


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


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


Control of breathing – prenatal development

fetal breathing

during REM sleep

depressed by hypoxia

(severe hypoxia -> gasping)

may enhance lung growth and development


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


Control of breathing – infantsVentilatory response to hypoxemia

first weeks (neonates)transient increase -> sustained decrease(cold abolishes the transient increase in 32-37 week premaures

by 3 weekssustained 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)


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


Central apnea

apnea > 15 seconds or

briefer but associated with

bradycardia (HR<100)

cyanosis or

pallor

rare in full term

majority of prematures


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 factorsextent of surgeryanesthesia techniqueanemiapostop 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


Upper airway - Larynx

three receptor typespressuredrive (irritant)flow (or cold)

response to stimulusapneacoughingclosure of glottislaryngospasmchanges in ventilatory pattern

newbornincreased sensitivity to superior laryngeal nerve stimulus ->

ventilatory depression or apneaH2O more potent stimulus than normal saline ([Cl-])


Infant (especially preterm) reflex response to fluid at entrance to larynx

Normal protectiveswallowingcentral apnea (H2O > NS)sneezinglaryngeal closurecoughing or awakening (less frequent)

During inhalation inductionpharyngeal swallowing reflex abolishedlaryngeal reflex intact ->

breath holding or central apneapositive pressure ventilation may ->

push secretions into larynx ->laryngospasm


Laryngospasm

Sustained tight closure of vocal cords by contraction of adductor (cricothyroid) musclespersisting after removal of initial stimulus

More likely (decreased threshold) withlight anesthesiahyperventilation with hypocapnia

Less likely (increased threshold) withhypoventilation with hypercapniapositive intrathoracic pressuredeep anesthesiamaybe 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


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


Rapidly adapting (irritant) receptors (RARs)

Especially carina and large bronchiStimulus

lung distortionsmokeinhaled anestheticshistamine

Responsecoughingbronchospasmtracheal mucus secretion

Likely mediate the paradoxical reflex of Head:with vagal afferents partially blocked by cold,inflation of lungs ->

sustained contraction of diaphragm withprolonged 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


C-fiber endings (J-receptors)

Juxta-pulmonary receptorsStimulus

pulmonary congestionedemamicro-emboliinhaled anesthetic agents

Responseapnea followed by rapid, shallow breathingbronchospasmhypersecretionhypotensionbradycardiamaybe 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


Peripheral Chemoreceptors

Carotid bodies3 types of neural components

type I (glomus) cellstype II (sheath) cellssensory nerve fiber endings

carotid nerve ->C.N. IX, glossopharyngeal nerve

StimuluspaCO2 and pHpaO2 (especially < 60 mmHg)

Response – increased ventilationContribute 15% of resting ventilatory driveNeonate: hypoxia depresses ventilation

by direct suppression of medullary centers


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)


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

50% of TLC =

= 25% TLC

= 60 ml/kg infant

after 18 monthsincreases to adult 90 ml/kgby age 5

may be only 15% of TLC in young infants under GAplus muscle relaxants


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 maintainednear values seen in older children and adults because of

1. continued diaphragmatic activity in early expiratory phase2. 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


Under general anesthesia, FRC declines by

10-25% in healthy adults with or without muscle relaxants and35-45% 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


General anesthesia, FRC and PEEP

Mean PEEP to resore FRC to normalinfants < 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:

R = 8lη/πr4where R resistance

l lengthη viscosity

For turbulent flow: 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%


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


Anesthetic effects on respiratory mechanics

Endotracheal tube adds the most significant resistance


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)


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


If SpO2 = 91

then = PaO2 =

Adult 606 months 666 weeks 556 hours 41


Implications for blood transfusion

older infants may tolerate somewhat lower Hgb levels at which

neonates ought certainly be transfused

P50 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


Surfactant

Essential phospholipid protein complexRegulates surface tensionStabilizing alveolar pressure

LaPlace equationP = nT/rwhere P ressure

r adius of small sphereT ensionn = 2 for alveolus

Surface tension: 65% of elastic recoil pressure

Pediatric Respiratory PhysiologySurfactant

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 PhysiologySurfactant

Synthesis increased byglucocorticoidsthyroxineheroincyclic adenosine monophosphate (cAMP)epidermal growth factortumor necrosis factor alphatransforming growth factor beta

Synthetic surfactant used in treatment ofpremature infants with surfactant deficiency PPHNCDHmeconium aspiration syndromeARDS (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

http://metrohealthanesthesia.com/edu/ped/pedAir.htm

http://metrohealthanesthesia.com/edu/ped/pedAir.htm

pediatric fundamentals. mcgraw-hill 2002 pediatric fundamentals objectives growth and development...

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