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
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