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Pediatric Respiratory Physiology. Drs. Greg and Joy Loy Gordon February 2005. Pediatric Respiratory Physiology. Prenatal – Embryo. Ventral pouch in primitive foregut becomes lung buds projecting into pleuroperitoneal cavity Endodermal part develops into airway alveolar membranes

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slide1

Pediatric Respiratory Physiology

Drs. Greg and Joy Loy Gordon

February 2005

slide2

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

slide3

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

slide4

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

slide5

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

slide6

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)

slide7

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

slide8

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

slide9

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

slide10

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

slide11

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

slide12

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

slide13

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

slide14

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)

slide15

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

slide16

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

slide17

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 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)

slide18

Pediatric Respiratory Physiology – Pulmonary and Thoracic Receptors

Upper airway

Pharyngeal receptors ->

inhibition of breathing

closure of larynx

contraction of pharyngeal swallowing muscles

slide19

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-])

slide20

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

slide21

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

slide22

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

slide23

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

slide24

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

slide25

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

slide26

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

slide28

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)

slide29

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

slide30

Pediatric Respiratory Physiology – Assessment of Respiratory Control

CO2 response curve

slide31

Pediatric Respiratory Physiology – Assessment of Respiratory Control

Effects of anesthesia on respiratory control

Shift CO2response 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)

slide32

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

slide33

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

slide34

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

slide35

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)

slide36

Pediatric Respiratory Physiology – Dynamic Properties

Poiseuille’s law for laminar flow:

where R resistance

l length

η viscosity

R = 8lη/πr4

For turbulent flow: Rα1/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%

slide37

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

slide38

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

slide39

Pediatric Respiratory Physiology

Oxygen transport

(Bohr effect)

= 27, normal adult (19, fetus/newborn)

slide40

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

slide41

Pediatric Respiratory Physiology

Oxygen transport

If SpO2 = 91

then = PaO2 =

Adult 60

6 months 66

6 weeks 55

6 hours 41

slide42

Pediatric Respiratory Physiology

Oxygen transport

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

Implications for blood transfusion

older infants may tolerate somewhat lower Hgb levels at which

neonates ought certainly be transfused

slide43

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

slide44

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

slide45

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)

slide46

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