pediatric respiratory physiology and respiratory distress and respiratory failure identification and management from a pediatric point of view

1. DR SAMEEKSHYA PRADHAN
GUIDE:ASSOC. PROF. DR. SANTISENA MISHRA

2. What is respiration?
 Respiration = the series of exchanges that
leads to the uptake of oxygen by the cells,
and the release of carbon dioxide to the
lungs
Step 1 = ventilation
 Inspiration & expiration
Step 2 = exchange between alveoli (lungs)
and pulmonary capillaries (blood)
 Referred to as External Respiration
Step 3 = transport of gases in blood
Step 4 = exchange between blood and cells
 Referred to as Internal Respiration
 Cellular respiration = use of oxygen in ATP
synthesis

3.  Respiratory system has 3
parts:-
I. Upper airway(nostril to
larynx)
II. Conducting airway(the 1st
16 divisons .i.e. from
trachea to terminal
bronchioles)
III. Alveolar airway(the last 7
divisons from
resp.bronchioles to alveolar
sacs)

5.  Small nostrils – easily occluded
 Small mouth larger tongue
 Larynx & glottis high up- increased risk of aspiration
 Chest wall more compliant.
 Ribs are more horizontal in children and diaphragm is
flatter...so upward and outward movt and downward
movt to expand lungs is not possible.
 fewer and smaller alveoli and so lung volume is less.

6. Produced by the type 2 pneumocytes
Composed mainly of
DPPC(dipalmitoylphosphatidylcholine) &
phosphatidyl glycerol.
Hyaline membrane disease(HMD)/
Respiratory distress syndrome(RDS):Seen
in premature babies leading to
atelectasis.
Maternal glucocorticoid treatment 24-48
hours before delivery accelerates lung
maturation and surfactant production

8.  It is the amount of air left in the lungs after tidal
expiration.
 FRC acts as a buffer, minimizing the changes in
PAo2 and PAco2 during inspiration and expiration.
 Represents the environment available for gaseous
exchange at all times.
 Decreased FRC(alveolar interstitial diseases and
thoracic deformities) Hypoxemia can be
corrected by ing PEEP.
 Both increased FRC(intrathoracic airway
obstruction) and decreased FRC (alveolar-
interstitial diseases) - cause decreased compliance
and increased WOB.

10. ELASTIC
WORK
•To stretch
elastic
tissues of
chest wall
and lungs
•65% of total
WOB
RESISTIVE
WORK
•To move air
through
airway
•25% of
total WOB
VISCOUS
RESISTANCE
•To move
inelastic
tissues
•7% of total
WOB
Welast is directly proportional to VT,where as
Wresist is determined by RR.

11.  Normal WOB= 0.3-0.8 kg.m/min(<3% of total
energy expenditure). This can increase to 40%
in CHF/CLD.
 WOB is lowest at a R.R of-
-35 to 40/min in neonates
-14 to 16/min in older child & adult
 ed compliance(as in alveolo-interstitial
disesase) Increased Welast. Shallow(low
VT) & fast respirations.
 ed resistance(as in obstructive airway
diseases) increasesd Wresist. Slow and
deep respirations.

12.  (ΔV/ΔP) for the whole lung at rest is about 0.8 (4.2
L/min ventilation 5.5 L/min blood flow).
 Due to gravity, alveoli in the apical region of lungs
are more inflated(so less compliant) in comparison
to alveoli in the dependent regions.So
ventilation(ΔV) is better at base.
 Due to gravity pulm.hydrostatic pressure increases
in the dependent regions so perfusion(ΔP) is also
more in dependent alveolois.
 But ΔV/ΔP- is more at apex than bases
Ventillation-better at apex
Perfusion-better at base

14. CLOSING CAPACITY:- lung volume at which the
dependent airways start to close.
-Normally FRC > CC
-In newborns : CC > FRC(so poorly ventilated
alveolis are perfused in tidal respiration l/t decreased PaO2
in newborns in comparison to older children)
VENOUS ADMIXTURE:- when
perfusion>ventilation, it leads to incomplete
arterialisation of venous blood.
INTRAPULMONARY(R->L) SHUNTING:- (e.g.
HMD, pneumonia,asthma)- perfusion of unventillated
areas occurs l/t complete shunting of venous blood
into arterial circulation.

15. DEAD SPACE VENTILATION:- Ventilation of
poorly perfused areas is wasted ventilation.
o This causes return of greater amounts of
atmospheric gas which has not participated in gas
exchange and has negligible CO2
o Occurs in states that result in decreased
pulmonary perfusion e.g. pulm.HTN,
pulm.thromboembolism,hypovolemia, decreased
cardiac output.

16.  When the interstitial space is filled with
inflammatory cells or fluid, diffusion is impaired.
 Diffusion capacity of CO2 is 20 times greater
than that of O2, diffusion defects manifest as
hypoxemia rather than hypercarbia.
as a result
-lethal hypoxemia will set in before
clinically significant CO2 retention results
-rather PCO2 decreases because of
hyperventilation
 Increased pCO2 here is indicative of alveolar
hypoventilation from coexisting airway
obstruction, exhaustion, or CNS depression.
 Ex: interstitial pneumonia, ARDS,
scleroderma,and pulmonary lymphangiectasia.

17. Respiratory rate and VT are regulated
by a complex interaction of-
-CONTROLLERS
- RECEPTORS &
- EFFECTORS

18. Involuntary voluntary
 Located in the
medulla & pons
 Directs the depth
and rate of
breathing via
outputs from the
respiratory centres
 May be modified
upon feedback
from other sites
 Located in the
cerebral cortex
 Sends impulses to
the respiratory
motor neurons via
the corticospinal
tracts
 Influential factors
include emotion,
pain

20. I. The pre-Botzinger complex (pre-BOTC).
 Rhythmic respiration is initiated by these
small group of pacemaker.
II. Dorsal Respiratory Group
 This is the inspiratory center.
 Firing leads to contraction of inspiratory
muscles
 When firing stops -> passive expiration
III. Ventral Respiratory Group
 Inactive during quite breathing
 During forced breathing or when the
inspiratory center is inhibited it becomes
active.

21. I. Pneumotaxic Center
 Basically decreases the duration of
inspiration.
 When this area is damaged, respiration
becomes slower and tidal volume greater.
II. Apneustic Center
 Basically acts to increase the duration of
inspiration.
 It is inhibited by pulmonary stretch
receptors through vagus nerve.
 So, if vagi are cut, apneusis(prolonged
inspiratory spasm) occurs.

23. Central
•Located on the
ventrolateral
surface of medulla
•Stimulated by
changes in pH in
CSF
•Co2 enters BBB-
changes to carbonic
acid- releases H+
ions- decreases pH
peripheral
•Located in the
Aortic & Carotid
bodies
•Detect decrease in
pO2 & Ph
•Increase the rate
and depth of
respiration.

24. 1.Stretch receptors
2.‘J’ receptors
3.Irritant receptors
4.Muscle receptors
5.Arterial baroreceptors
6.Pain and temperature receptors

25. Main muscles:-
diaphragm, intercostals & abdominal
muscles
Accessory muscles:-
sternocleidomastoids and paraspinal
muscles

27.  SIGNS:-
I. Nasal flaring
II. Lethargy
III. Tachypnoea
IV. Chest wall retraction
V. Stridor
VI. Grunting
VII. Dyspnoea
VIII.Wheezing

28. 1) NASAL FLARING:-V.imp sign of distress(esp.
In infants). It indicates discmfort,
pain,fatigue,breathing difficulty.
2) DECREASED RESPONSIVENESS:- S/o
impending resp. Failure.
3) CHANGE IN RATE & DEPTH OF
RESPIRATION:-
 ed lung complince -> rapid & shallow
Obstructive diseases -> slow & deep
Non-respiratory causes -> rapid & deep
(metabolic acidosis, CNS stimulation)

29. 4. CHEST WALL RETRACTION:- s/o increased
inspiratory effort or weak chest wall or both.
5. INSPIRATORY STRIDOR:- s/o airway obstruction
above thoracic inlet(e.g.laryngomalacia,
choanal atresia, laryngotracheobronchitis).
6. EXPIRATORY WHEEZE:- s/o airway obstruction
below thoracic inlet.
7. GRUNTING:- produced by expiration against a
partially closed glottis and is an attempt to
maintain PEEP for as long as possible.
-occurs in diseases with decreased
FRC(such as in pulmonary edema, hyaline
membrane disease,and pneumonia) & also in
bronchiolitis(to prevent airway collapse).

30. (choanal atresia ,retropharyngeal abscess, laryngotracheobronchitis )

31. (vascular ring,mediastinal tumors)

32. (asthma, bronchiolitis)

36.  Respiratory failure is defined as inability of
the lungs to provide sufficient oxygen
(HYPOXIC RESPIRATORY FAILURE) or remove
carbon dioxide (VENTILATORY FAILURE) to
meet metabolic demands.
 Although respiratory failure is traditionally
defined as respiratory dysfunction resulting
in Pao2 <60 torr with breathing of room air
and Paco2 >50 torr resulting in acidosis,
the patient’s general state, respiratory
effort, and potential for impending
exhaustion are more important indicators
than blood gas values.

37. Abnormality in:-
1. Lungs and airways
2. Chest wall & muscles of respiration
3. Respiratory control

41. Type I (Hypoxic
resp.failure)
 Occurs in conditions
with
-venous admixture
-intrapulmonary shunting
-diffusion defects
 Examples-
-small airway obstruction
-ARDS
-Pneumonia
-Pulm.edema
 a/w deceased FRC
 Can be Managed by
increasing PEEP.
Type II (Hypercarbic
resp.failure)
 Occurs in conditions
with
-ventilation defects
-increased dead space
ventilation
 Examples
-decreased CNS
respiratory drive
-obstuctive airway
disease

42. TYPE I TYPE II
 Pao2<60, PaCO2- N/low
ACUTE CHRONIC
. H - N/ N
.HCO3- N N
 PaO2<60, PaCO2>50
ACUTE CHRONIC
. H - N/
.HCO3- N

43.  ACUTE TYPE I
RESPIRATORY FAILURE
Examples-
• Acute asthma
• Pulmonary edema
• Pneumonia
• Pneumothorax
• ARDS
• Pulmonary embolism
 CHRONIC TYPE I
RESPIRATORY FAILURE
Examples-
• Rt to lt shunts
• Chronic pulm. Edema
• Chronic pulm
thromboembolism
• Lung fibrosis
 ACUTE TYPE II RESPIRATORY
FAILURE
Examples-
• Respiratory depressant drugs
• Spinal cord disorders(GBS,Polio,
myaesthenia)
• Acute neuropathies/paralysis
• Severe airway obstruction(severe
ac.asthma,laryngeal/tracheal
obstruction)
 CHRONIC TYPE II RESPIRATORY
FAILURE
Examples-
• Sleep apnea
• Kyphoscoliosis
• Ankylosing spondylitis
• Myopathies/muscular dystrophies
.

44. Acute lung injury due to pneumonia,
sepsis,aspiration,drowning,embolism,
trauma, smoke inhalation, or drug
overdose may lead to the ARDS.
Clinically, A-aO2 gradient >200 is
characterized as acute lung injury
and a gradient >300 is termed as
acute respiratory distress syndrome
(ARDS)

47. 1) Clinical examination
2) Pulse oximetry
3) Capnography
4) Blood gas analysis.

48.  Most important method
 Asses the signs of respiratory distress & their
progression & relation to t/t.
 The child with respiratory distress or failure
should be observed in the position of
greatest comfort and in the least threatening
environment.

49.  MC method used to monitor oxygenation.
 Non-invasive and safe.
 It measures the %age of oxyHb in arterial blood.
 A pulsatile circulation is required.
 Spo2 value greater than 95% is a reasonable goal, especially in
emergency situations.
Inaccurate in -
 CO poisoning
 Methemoglobinemia
 Shock,cardiac arrest
 Finger nail polish
 Excessive light
 Low Hb
 IV dyes
 Pulse oximetry should not be the only monitoring method in
patients with primary ventilatory failure like NM weakness and
CNS depression (as with supplemental O2, SpO2 is good in such
cases but dangerous hypercarbia may go undetected).

50.  Measures end-tidal CO2.
 especially useful for monitoring the level of
ventilation in intubated patients.
 Diseases resulting in increased dead space or
decreased pulmonary blood flow lead to
decreases in ETCO2 and hence overestimate
the adequacy of ventilation.

51.  Types- ABG,CBG,VBG
• Useful in emergency situations.
• A properly“arterialized” CBG sample
obtained by warming the digit and
obtaining free flowing blood is acceptable
which needs to be processed without
delay.
• CBG provides a good estimate of Paco2
and arterial pH, but less so for pO2.

52. • In patients whose oxygenation is being
monitored with pulse oximetry,VBG sample
provides reliable estimate of adequacy of
ventillation.
• Measures pCO2 & pH reliably,but poorly
correlates with Po2
• Venous pCO2 is approximately 6 torr higher
and pH approximately 0.03 lower than the
arterial values.

53.  Baseline values-pH 7.40,Pco2 40mm & HCO3-24 mEq/L
In newborns- pH 7.38, Pco2 35mm & HCO3- 20 mEq/L.
 Metabolic acidosis with respiratory compensation-
-Normal compensation: results in a fall in Pco2 by 1.2mm
for every 1 mEq/L fall in HCO3
- Quick method: look at the last 2 digits of pH (provided it
is not below 7.10) which should be within 2mm of Pco2
-Winter’s formula: Paco2 = (HCO3 × 1.5) + 8 + 2
 Respiratory Acidosis with Metabolic Compensation-
-An acute increase in Pco2 of 10mm results in a decrease in
pH by 0.08.
- Chronically elevated (greater than 3-5 days) Paco2 is
accompanied by renal compensation limiting the fall in
pH to 0.03 for every 10 mm rise in Paco2.

55. 1. To maintain airway.
2. To provide O2 support.
3. To enable CO2 removal.
4. Prompt diagnosis and management of underlying
cause.
Hypoxemia is more life threatening than hypercania-
so, 1st adequate oxygenation must be ensured.

56. • Nasal cannula
• Simple face mask
• Venturi mask-
• Partial rebreathing mask-(FiO2-60%)
• Non –rebreahing mask-(FiO2-95%)
• Oropharyngeal airway
• nasopharyngeal airway.

57.  HELIOX- Mixture of helium(60%) and
oxygen(40%).
-low density, so decreases turbulence
-helpful in large airway obstruction and
status asthmaticus.
-can’t be used if patient needs >40% O2.
 NITRIC OXIDE- is a pulmonary vasodilator.
- may improve pulmonary blood flow
and V/Q mismatch in patients with diseases that
elevated pulmonary vascular resistance, such as
PPHN, primary pulmonary HTN, and secondary
pulmonary HTN.

58. CPAP- continuous positive airway pressure
BiPAP- Bilevel positive airway pressure
machines provide positive airway pressure
during exhalation and additional positive
pressure during inspiration.
When hypoxemia or significant
hypoventilation persists despite all above
methods tracheal intubation and mechanical
ventilation are indicated.