PAEDIATRIC RESPIRATORY

PHYSIOLOGYPART 1

DR. PRIYANKA KARNIK

Objectives: To understand

Embryology and development

Prenatal development of breathing and perinatal adaptation

Control of breathing

Maintenance of airway and protective reflexes

Effects of anaesthesia

Lung volumes

Mechanics of breathing

Embrology

Ventral pouch in primitive foregut becomes

lung buds projecting into pleuroperitoneal cavity

Endodermal part develops into

alveolar membranes

mucous glands

Mesenchymal elements develop into

smooth muscle

cartilage

connective tissue

lymph vessels

Pseudoglandular period: until 17th

week of gestation. Preacinar

branching upto terminal bronchioles

Disturbance of expansion at this stage

as in CDH results in hypoplasia.

Canalicular stage: upto the respiratory

bronchioles

Terminal sac(alveolar period): clusters

of terminal sacs with flattened

epithelium- 24th week

Microvascular development: 26th-28th

week

Alveolar formation: as early as 32nd

week, however most alveolar

formation postnatally 12th – 18th

months of life

At birth: 20-50 million terminal air sacs

but only 10% fully grown.

Type 2 pneumocytes at 24th- 28th

week

Surfactant

Produced by the type 2 pneumocytes

Hyaline membrane

disease(HMD)/Infant respiratory

distress syndrome(IRDS): Seen in

premature babies.

Maternal glucocorticoid treatment 24-

48 hours before delivery accelerates

lung maturation and surfactant

production

Fetal lung produces large amount of

fluid which expands the airway as the

larynx is closed

Growth factor(human bombesin) which

stimulates development

Occlusion of trachea tried in CDH to

promote growth of hypoplastic lung

Perinatal control of breathing

Respiratory rhythmogenesis occurs not at birth but in utero

30-31 weeks: 58breaths per minute

near term fetus: 47breaths per minute

Helps in development of lung due to stretching of lung tissue.

Abolished by hypoxia, maternal alcohol ingestion and cigarette smoking

Independent of paCO2

Clamping of umbilical cord at birth

rhythmic breathing

Relative hyperoxia with air breathing initiates and maintains breathing

30-70cms of water pressure required to expand fluid

filled lungs

PVR decreases due to lung expansion

Markedly increased pulmonary blood flow :

increased left atrial pressure with closure of

foramen ovale

Control of breathing(neural)

Dorsomedial respiratory group:

inspiratory

medulla

Ventrolateral respiratory group:

expiratory

Pontine group: rapid breathing

Pre Botzinger complex: rhythmic

breathing

Control of breathing(chemical)

Central chemoreceptors:

ventrolateral medulla

Changes in the H+ ion conc in the adjacent CSF

Peripheral chemoreceptors:

Bifurcation of common carotid carotidartery

Changes in arterial paO2 (especially < 60 mmHg)

Receptors

Upper airway receptors:

Stimulation of receptors in the nose produces sneezing,

apnea, changes in the bronchomotor tone and diving

reflex.

During swallowing, there is inhibition of breathing,

closure of larynx and coordinated.

Tracheobronchial and pulmonary receptors

Slowly adapting(pulmonary stretch receptors)-

membranous posterior wall of trachea and

central airways

Hering breuer inflation reflex

apnea due to inflated ETT cuff

Rapidly adapting(irritant or deflation): situated

in carina and large airways

Hering breuer deflation reflex-increase in

respiratory drive at low lung volumes as in

IRDS and pneumothorax.

also mediate paradoxical reflex of head- deep

inspiration instead of inspiratory inhibition

Helps to inflate the unaerated portion of

newborn lung

C fibre endings: near the pulmonary capillaries

Stimulated by pulmonary congestion, microemboli, pulmonary edema, anaesthetic gases

Such stimulation leads to apnea followed by rapid shallow breathing, hypotension and bradycardia

Reflex contraction of the laryngeal muscles responsible for laryngospasmduring isoflurane induction

During first 2-3 weeks of life, both full term and

preterm neonates respond to hypoxemia(<15%

oxygen)- transient increase in ventilation f/b

ventilatory depression

Hypercapnia- increasing ventilation

Periodic breathing- breathing interspersed with

short apneic spells lasting 5-10s without

desaturation or cyanosis.

Incidence about 78% in full term and 93% in

preterm neonates.

may be abolished by adding 2-4% CO2 to inspired

gas

Decreases to 29% by 10-12 months of age.

Apnea of prematurity

Central apnea of infancy- cessation of

breathing for15s or longer or a shorter

pause associated with bradycardia,

cyanosis or pallor.

<2kg preterm infants

immature respiratory control mech

55% incidence.

Post op apnea

Preterms < 41 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 55 weeks PCA(Kurth

1987)

Associated factors: extent of surgery,

anesthesia technique, anemia ,postop

hypoxia

Risk of apnea decreases to <5% in

PCA> 44(Cote 1995)

Much less seen with sevo and

desflurane

General consensus: overnight

observation for <44 weeks PCA.

Caffeine and theophylline for reduction

Pharyngeal airway

Pharyngeal airway is not supported by a rigid, bony or cartilaginous framework

Made up of soft tissues and muscles for breathing and swallowing

Collapsing forces acting on the airway: luminal negative pressure during inspiration, sedation, paralysis

Pharyngeal dilator forces: genioglossus, geniohyoid, hypercapnia and hypoxemia

Negative pressure in the nose pharynx and airway activates the dilator muscles and decreases diaphragmatic activity

Such an airway reflex present in infants<1 yr of age

Laryngeal airway

Larynx at the subglottis is narrowest of

entire airway

Cylindrical in shape rather than funnel

shaped.

The cricoid opening is not circular but

mildly elliptical with a smaller

transverse diameter

Recent trend of favouring cuffed ETT

over uncuffed ETT

Glottis widens during inspiration and narrows during expiration, increasing the laryngeal airway resistance which maintains the FRC

Grunting seen during expiration in IRDS-maintains the iPEEP, prevents premature airway collapse

If this pt is intubated, grunting is eliminated and gaseous exchange deteriorates to the point of cardiac arrest unless CPAP is applied.

Airway reflexes

Sneezing, coughing, swallowing,

pharyngeal and laryngeal closure

Laryngospasm:

Sustained tight closure of vocal cords

caused by the stimulation of superior

laryngeal nerve.

by contraction of adductor

(cricothyroid) muscles

persisting after removal of initial

stimulus

Laryngospasm

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)

Tretment of laryngospasm

Removal of stimulus

100% oxygen with CPAP

Larson’s manouvre at the laryngospasmnotch: skull superiorly, mastoid process posteriorly and angle of mandible anteriorly

Deepening of plane of anaesthesia (20% of the induction dose)

Suxamethonium 0.5mg/kg

Atropine 0.01mg/kg for bradycardia

Intubate if required

Lung volumes

Early period of postnatal life, lung

volume of infants is disproportionately

small in relation to body size

Metabolic rate and O2 requirement is

twice that of an adult.

Much less reserve of lung volume and

and surface area for gas exchange

Rapid desaturation

FRC

Determined by the balance between outward recoil of the thorax and inward recoil of the lungs

50% of TLC in upright position and 40% in supine

In anaesthetised paralysed conditions it becomes 10-15% of TLC.

Outward recoil of thorax is extremely low in infants due to cartilaginous ribs and horizontal rib cage while inward recoil is only slightly low

Maintenance of FRC

Sustained tonic activities of inspiratory

muscles throughout the respiratory

cycle

Breaking of expiration with continual

but diminishing diaphrgmatic activity

Narrowing of glottis during expiration

Inspiration starting in mid expiration

High respiratory rate in relation to

expiratory time constant

TLC

Maximum lung volume allowed by

strenth of inspiratory muscles

stretching the thorax and lungs

60ml/kg in infants

By 5yrs of age, reaches 90ml/kg

Effect of anaesthesia

Average decrease in the FRC is about 46% among those less than 12 yrs of age.

To restore FRC to the normal portion of PV curve, a PEEP of 5-6cm of H2O has to be added for infants<6 months and 12cms in older children

Compliance decreases to about 35% Persistent airway closure during

anaesthsia leads to resorptionatelectasis and V/Q mismatch and reduced arterial pO2

Hence supplemental O2 in the PACU

Elastic properties

Lung compliance=∆V/∆P

where ∆V is tidal volume and

∆P is the transpulmonarypressure(difference between airway and pleural pressure)

Compliance of infant lungs is very high as elastic recoil is low due to absent or poorly developed elastic fibres

Prone to airway collapse ( just like the emphysematous geriartric lungs)

Airway resistance

The resistive properties of the respiratory system include

Resistance of air flow within airwaysi. Tissue viscoelastic resistance(

resistance of lung and thoracic tissues to deformation)

ii. Inertial resistance( due to movement of gas within the airways)

During tidal breathing, inertance is very low

90%work to overcome elastic forces and 10% to overcome flow resistance

Distribution of resistance

In the newborn airway resistance is very high (19 to 28 cm H2O/L per sec) and decreases to less than 2cm H2O/L per second

Upper aiways: extrathoracic

65% of total airway resistance

Lower airways: intrathoracic

35% of total airway resistance

Of this central airways(trachea, large bronchi) account for 90% of resistance

Peripheral airways( small bronchi, bronchioli) account for only 10% of resistance.

Flow resistance= 8nl/πr4

above equation holds true for laminar

flows ie quiet tidal breathing

In turbulent flows, however, the

resistance increases by r5.

Inflammation or secretions in the

airway results in exaggerated degrees

of obstruction in airway and increases

work of breathing

Time constant

When the lung is allowed to empty passively from end inspiration to FRC, the speed of lung deflation is determined by the product of resistance and compliance.

This is the unit of time ie time constant

t= R*C

It requires 3 time constants to nearly complete exhalation.

In healthy children and adults, t is 0.4-0.5s and in neonates it is 0.2-0.3s

It is increased in pts with obstructive disease and pts breathing through ETT

Hence more time to be given for expiration