Respiratory Physiology - Pediatric Anesthesia

1. Respiratory Physiology in
Infants and Children
Presenter : Dr. Sphurthy
Moderator : Dr. Swathi

2. Introduction
• Respiratory physiology is different in neonates, infants and young children from
that of older children and adults.
• 70–80% of morbidity and mortality - perioperative period - respiratory
dysfunction.
• To apply appropriate anaesthetic principles & improve perioperative outcome in
paediatric patients

3. Control of breathing – Infants vs Adults
Ventilatory response to hypoxemia :
• Up to 3 weeks - transient increase in ventilation followed by sustained ventilatory
depression.
• Attributed to central depression rather than to depression of peripheral
chemoreceptors.
• Transient hyperpnea - abolished in a cool environment. (hypothermia)
• By 3 weeks, hypoxemia induces sustained hyperventilation - older children and
adults.

4. • Chemoreceptor
responses
- blunted in preterm.
• Biphasic response
- replaced by apnoea .

5. Ventilatory Response to hypercapnia
• Newborn infants - increase ventilation.
• But less so than do older infants.
• With hypoxemia, CO2 response curve :
Adults – increased slope, left shift
Infants – decreased slope, right shift
• The slope increases - gestational age and postnatal age.
• Independent of postconceptional age.

6. Hypoxia depresses
hypercapnic
ventilatory responses –
young infants.

8. Effects of anesthesia on
control of respiration
Shift CO2 response curve to right

9. Periodic breathing
• In quiet and active sleep
•Both preterm and healthy term neonates
• Infants have an irregular and periodical breathing pattern
• Different from clinical apnoea
• Apneic spells, 5 - 10 seconds, without cyanosis or bradycardia
• 93 % - preterm,78 % - full term, 29 % - 10 to 12 months
• May be abolished by adding 3 % CO2 to inspired gas

10. APNEA – TYPES OF APNEA
1. Central apnea / Apnea of prematurity
DEFINITION
• Cessation of breathing > 20 seconds
• Less than 20 seconds, associated with
bradycardia (HR < 100/min)
cyanosis or
pallor / hypotonia

11. Why - Central Apnea..???
Due to immature respiratory control mechanism
• hypoxic ventilatory depression
• diminished hypercapnic response
• active inhibitory reflexes
An infant born at a lower post conceptional stage - more likely to have apnea than
one with same post conceptional age but born later.
• Preterms < 44 weeks postconceptional age - risk of apnea is 40 - 50 %
• > 44 weeks PCA - decreases significantly (to 5%) but still exists.

12. Central Apnea..
• Exacerbating factors – hypoxia, sepsis, intracranial haemorrhage, metabolic
abnormalities, hypo/hyperthermia, upper airway obstruction, heart failure,
anaemia, prostaglandins and anaesthetic agents
• ALTE – apnea, color change, tone, choking / gagging ( 3%, previously healthy
also)
• Treatment – stimulation, bag-mask ventilation, treat underlying abnormalities,
caffeine or theophylline, neonatal CPAP or ventilation.

13. CAFFEINE
• 5 to 10 mg/kg, IV – pre / intra / postoperatively
• Significantly reduces postoperative apnea.
1. Stimulates the respiratory center
2. Enhances responsiveness to CO2,
3. Increases diaphragmatic contractility,
4. minute ventilation
• Oxygen consumption and metabolic rate - effects
• Reduction in duration of CPAP - observed.
• Neurodevelopmental outcomes – improved.
• Problem - lower weight gain + increased incidence of death.
• A recent study advocated its administration to only infants weighing <1250 g.
(Fakoor et al, 2019)

14. Post-operative Apnea in Preterms
Central Apnea continues…
• Usually - within 12 hours postoperatively
Significant risk factors
• Postoperative hypoxemia
• Hypothermia
• Anemia (Hematocrit < 30 is the most important) regardless of gestational or
postconceptual age
Less with newer anesthetic agents e.g., sevoflurane or desflurane

15. Other types of Apnea
2. Obstructive apnoea
Opposition of hypopharyngeal soft tissues / nasal occlusion
3. Mixed apnoeas
Obstruction followed by central pauses ( most frequent )

16. MECHANICS OF BREATHING

17. MECHANICS OF BREATHING
2-7 ribs, move simultaneously on two axes
“Pump handle” motion - Rotate on axis of neck - sternal end, increases AP
diameter
“Bucket handle” - Along long axis : middle part of the rib moves up and
down

18. Thoracic wall - highly compliant
Lung tissue – poorly developed elastic fibres
Muscles - less developed, little structural support
Boxlike cage, ribs horizontal
Diaphragm - horizontal plane, decreased effective expansibility
Also, larger abdominal visceral content

19. COMPLIANCE
Defined as change in lung volume per unit change pressure gradient
• C = ∆V / ∆P
• Determined by :
Elastic forces of lung tissue
Alveolar surface tension

20. Lung compliance depends on lung volum
Lowest at extremely low or high FRC

21. C static = Tidal volume / (Plateau pressure - PEEP)
• Airflow is absent.
• Reflects the elastic resistance of the lung and chest wall
C dynamic = Tidal volume / ( Peak inspiratory pressure – PEEP)
• Airflow is present.
• Reflects the airway resistance + elastic resistance of airway and chest wall.
• Obstructed lungs – frequency dependence of compliance

22. • Decreased dynamic compliance with normal static compliance - acute increase
in airway resistance.
Assessed further, by comparing peak pressure and plateau pressure.
May be secondary to endotracheal tube obstruction, mucous plugging,
bronchospasm.
• If volume is constant, acute changes in both dynamic and static compliance –
worsening pneumonia, ARDS, atelectasis or increasing abdominal pressures.

23. COMPLIANCE – in neonates & infants
Elastic Properties of Lung continues…
• Neonates, chest wall compliance, CW = 3-6 x CL , tending to decrease FRC.
• By 9-12 months, same as adults, CW = CL .
• 1/Crs = 1/ CL + 1/CW
• During artificial ventilation, in adults, inspiratory pressure is equally distributed to
expand lungs and chest wall.
• In neonates and infants, chest wall - extremely compliant  requires little
pressure to expand  airway pressure should be reduced.

24. • Left
dashed
line – Cw
• Extremely
compliant

25. Developmental changes – Lung & Chest wall
• Lungs : Elastic recoil – low ; Compliance – high.
• Chest wall : outward recoil – low (hori ribs,less m/s)
• After neonatal adaptation – high CL.
• CL decreases with age as elastic recoil increases.
• Absolute terms : CL – increases with size of body

26. In preterms & Young Infants, P pl - slightly negative or nearly atmospheric  decreased FRC.
FRC dynaminally maintained by
• Sustained tonic activities of inspiratory muscles throughout the respiratory cycle
• Breaking of expiration - continual but diminishing diaphragmatic activity
• Narrowing of the glottis during expiration – Laryngeal braking
• Inspiration starting in mid-expiration
• High respiratory rate in relation to expiratory time constant
By 12 months, passively maintain FRC (CW = CL)
All mechanisms of sustaining FRC are lost - anesthesia or muscle relaxant

28. In IRDS, expiration - associated with “grunting” -
• Maintains intrinsic positive end-expiratory pressure (PEEP)
• Attenuates reduction in FRC
• Prevents premature closure of airways and air spaces.
Endotracheal intubation - eliminates auto PEEP  worsens respiratory gas
exchange, rapidly & critically  cardiorespiratory arrest ( unless CPAP applied )

29. Anaesthetic effects : General anaesthesia, FRC and PEEP
• General anaesthesia blunts laryngeal braking  decreased FRC  airway
closure  atelectasis  V/Q mismatch  R to L shunting  fall in PaO2
GA  C cw - decreases, CL – normal
FRC decreases by 30 % (adult )
46 % (children)

30. GA with/without MR
• 1973, Westbrook et al, adults, Thiopentone + dTc – 25 % fall FRC
• 2006, Von Ungern Sternberg et al
< 6 months – 43 % fall FRC ( collapse of highly compliant chest wall )
toddlers – 10 % fall FRC

31. Anaesthetic effects : General anaesthesia, FRC and PEEP
Transport to PACU

32. Anaesthetic effects : General anaesthesia, FRC and PEEP
• PEEP -- essential in infants < 9 months ; important in children < 3 years
• Infants < 6 months -- 6 cm H2O
Children – 6 to 12 cm H2O
• Under GA + muscle relaxants, PEEP increases total compliance by 75%
• Reduced lung volume + high O2 consumption = profound hypoxemia.

33. Anaesthetic effects : General anaesthesia, FRC and PEEP
• Closing volume (CV) - lung volume above RV at which airflow during expiration
ceases from dependent lung zones
• Collapse of small airways
CC = CV + RV
• Closing volume is higher than FRC (as % of FRC ) in infants and young children (
recoil high ).
• Infants modify respiratory mechanics to maintain small airway patency by auto‐PEEP.
• CV - Increases with age

34. Surface Tension
Elastic Properties of Lung continues…
• Defined as attractive force exerted - on the surface molecules of a liquid - by the
molecules of liquids beneath - that draws the surface molecules into the bulk of the
liquid to make shape having least surface area.
• When water forms a surface with air, the water molecules on the surface of the water
attract one another.
• Alveoli try to collapse

35. Surfactant
Surface Tension continues…
• Secreted by type II alveolar epithelial cells.
• Mixture of several phospholipids, proteins, and ions.
• The most important components are the phospholipid –
dipalmitoylphosphatidylcholine & glycerine
surfactant apoproteins
calcium ions.

36. Surface Tension
Elastic Properties of Lung continues…
• If the air passages are blocked, then surface tension tries to collapse the alveoli.
• Pressure in occluded alveoli - caused by surface tension.
• This creates positive pressure in the alveoli, attempting to push the air out
• The amount of pressure generated in alveolus - P = 2T/R ( Laplace’s law)
• Premature babies have little or no surfactant
• 6 - 8 times tendency to collapse – RDS.
• Fatal if not treated ( CPAP )

37. 37

38. Resistive Forces Opposing Lung Inflation
1 ) Tissue viscous resistance
2) Airway resistance
3) Inertance ( high velocity of movement of gases )

39. Tissue Viscous Resistance
• Caused by displacement of tissues during ventilation
• Displaced tissues - lungs, rib cage, diaphragm, and abdominal organs
• Only 20% of the total resistance to lung inflation
• Obesity, pleural fibrosis, ascitis

40. Airway Resistance / Flow resistance
• Caused by movement of gas through airways
• 80% of the total resistance to ventilation
R = ∆P / ∆V = ∆P/F

41. Factors Affecting Resistance
• Laminar flow and Turbulent flow
• Poiseuille’s equation - for gas flow to remain constant, pressure is directly
proportional to length and inversely proportional to the fourth power of the
airway’s radius.
V = P∏r4 / 8րL
V=flow rate, P=pressure gradient, r=radius, ր=viscosity, L=length
• RESISTANCE = 8րL / ∏r4

42. Airway Resistance / Flow resistance
• By reducing the
radius by half, 16-
fold pressure
increase to
maintain constant
flow
• Narrow airways -
large increase in
driving pressure -
markedly increases
in WOB

43. Distribution of Resistance
• 80% - nose, mouth, and large airways - turbulent flow
• 20% - airways smaller than 2 mm in diameter - laminar flow
• Contradict ? - resistance inversely related to radius
Branching - cross-sectional area with each airway generation

44. Distribution of resistance
Lower airways: intrathoracic,
35% of total Raw
• Central (large) airways:
trachea, large bronchi. 90% of
lower Raw (30%)
• Peripheral (small) airways:
small bronchi, bronchiole. 10%
of lower Raw (<5%)

45. Distribution of Resistance
Upper airway resistance –
• Mouth/nose, pharynx, larynx (the narrowest segment)
• 2/3 of total resistance
Adults, nasal - 65 % of total resistance
Infants, nasal - 30-50 % of total
NG tube increases total resistance up to 50 %
Endotracheal tube adds the most significant resistance

46. Raw and Rvisc – flow & volume dependent
Raw – increase with increasing flow,
decrease with increase vol ( airway calibre )
Rvisc – decrease with increase flow @ constant vol.
increase with increase volume @ const. flow
• Airway obstruction – old concept, to allow exhalation,
high TV, low RR – avoid PEEP.
Now, small TV, high RR – decrease R -> WOB
• Flow R – absolute – R max in small upper airway
 Obstruction
• Relative to body size, airway is big only  R in infants is less 
increases rapidly by 1 year, alveoli are formed.
Rvisc – larger contribution to total R

47. Time constant
• When lungs allowed to empty to  end expiratory FRC
• Speed of deflation
• T = C х R
• At 1 TC, TV decreases by 63 %
• Takes 3 TC to come to FRC
• Healthy adults & children – 0.4 to 0.5 sec
• Neonates – 0.2 to 0.3 sec
• TC increases – GA with ETT

48. Obligate nasal breathers – why ?
• Large tongue, small oral cavity  airflow obstruction - sleep/ sedation
• Epiglottis – long, omega- shaped, horizontally, high in pharynx, very close to soft
palate
• Absent paranasal sinuses - LESS RESISTANCE in nose
• Nasal passages – small  Easily obstructed – secretions/edema  increase WOB
• Mouth open during mask ventilation
• Over months to years, Mandible – rapidly grows, oral cavity larger in older infants
and children, laryngeal structures descend & separate epiglottis from soft palate 
transit from obligatory nasal to oral breather

49. Maintenance of the Upper Airway
Both in pharynx and larynx :Upper airway mechanoreceptors
Located superficially in the airway mucosa
• sneezing,
• swallowing, Easily blocked by topical anesthesia
• coughing,
• Pharyngeal, laryngeal closure
Sleep, sedatives, anesthesia depress upper airway muscles >>
diaphragm

50. Sustainance of Pharyngeal Patency :
Suction (collapsing) force - in
pharyngeal lumen – by inspiratory pump
muscles (diaphragm)
Mechanical support by pharyngeal
airway dilator muscles
Partial obstruction - exaggerates the
suction force
Maintenance of the Upper Airway

51. Effects of anesthesia
• General anaesthetics, opioids, sedatives - depress ventilation
• All inhaled anaesthetics significantly depress ventilation ( dose-dependent )
• Depress genioglossus, geniohyoid, other pharyngeal dilator muscles 
upper airway obstruction (infants  adults)
increased work of breathing
• Decreased with
Chin lift / Jaw thrust, CPAP 5 cmH2O
Oropharyngeal / Nasopharyngeal airway, LMA

52. Supraclavicular and intercostal retractions –
• During inspiration.
• Inward movements of the soft tissues above clavicle & between ribs
• Due to decrease in intrathoracic and pleural pressure  “sucks” soft tissues
inwards.
• Increase work of breathing.

53. ODC

54. ODC – Implications

55. ODC – Implications
Oxygen transport
Bohr effect :
increasing pH (alkalosis) decreases P50
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

58. TAKE HOME POINTS

59. REFERENCES
• Smith’s, 9th Edition
• Miller’s Anesthesia , 8 th Edition
• Egan’s Fundamentals of Respiratory Care, 11th Edition
• Respiratory Physiology, The Essentials – John B West
• Guyton and Hall, Textbook of Medical Physiology.

60. Thank You 