PHYSIOLOGIC

DEVELOPMENT
NEONATAL & PEDIATRIC
RESPIRATORY CARE
OLFU College of Respiratory Therapy
D. B. ADUL, M.D.

TRANSITION PERIOD: Pulmonary

Circulation
Fetal bld flow to the lung: 1/5
1/10 the amount found in
extrauterine life
Fetal lung: not an organ for
gas exchange
Blood is shunted away fr. The
lung thru the ductus arteriosus
Rt. Ventricular output goes
from PA to aorta
Diminished amount of bld that
returns from PV to LA also
joins the blood in the aorta

O2 bld placenta
umbilical vein ductus
venosus RA FO
LA LV aorta
Inc. resistance to bld flow
in arterial bed of lung
Resistance may be inc.
by hypoxia
Reduced by inc. 02 &
dec. C02 or H+ concn. In
pulm. Art. Bld.

At birth.
Lungs are inflated w/ air
Mechanical expansion dec. pulmonary vascular
resistance due to changes in 02, C02 and pH
Bld flow inc. in lungs more bld returned to LA inc.
LA pressure foramen ovale closes
Fetal bld flow: R to L at birth, bld flow L to R DA
closes
FO & DA closes soon after birth but may reopen in days
after birth
FO: responsive to pressure changes bet. 2 atria
DA: responds to p02 & prostaglandin levels
May be manipulated by using indomethacin to close or
PGE2 to open it

FETAL LUNG FLUID

Fetal lung is filled w/ fluid (30ml/kgBW)
Necessary component of fetal lung growth
There must be some distension of lung by fluid for
the lung to develop normally

Secretion can be dec. by carbonic anhydrase

inhibitor & stopped by cyanide
Epinephrine dec. secretion
At birth: secretion stops liquid is absorbed in
lymphatic system & interstitium of lung
Represents a handicap to air breathing but is
replaced by air at birth w/o problems

Determination of lung development

Too little amniotic fluid due to amniotic fluid
leaking or dec. urine production
underdeveloped/hypoplastic lung.
Oligohydramnios Potters syndrome
Group of anomalies: oligohydramnios sequence
Pulmonary hypoplasia
Fetal compression (flattened face & extremities)

Dec. fetal breathing movements

underdeveloped lungs
Dec. thoracic space diaphragmatic hernia
Small or poorly developed lungs

 Hormones can have an effect on growth of lung

Cortisol principal hormone
(+) structured lung development & production of
surfactant

Factors that stimulate lung maturation

ACTH, thyroid hormones, estradiol, prolactin,
epidermal growth factor, PG

Insulin & testosterone: (-) surfactant synthesis

Lung Inflation at Birth

Fetal respiratory movements: sign of fetal wellbeing
Respiratory movements not continuous, occur in
bursts of activity
May be depressed by drugs or anesthesia
Impt. To development of lungs & resp. muscles of
fetus

30 mins after birth: aerated lungs (term)

FRC: 95% ; initial respiratory volume 20-70ml
Initial residual volume: 20-30ml
Preterms: inc. effort to inflate lungs, tends to deflate

 1st wk of life:
Inc. in compliance from 2ml/cmH20 to 4-6ml/cmH20
(related to surface tension)

Stimulus for NB to breathe: factors

Cutaneous stimuli
Major stimulus: dec. 02, inc. C02

CS delivery: NB has no effort to breathe for 1st

seconds
Exerts more effort on initial expansion of lungs
May have some signs of respiratory distress
May hear rales on auscultation but cleared in few
mins.

Summary
Fetal lung fluid at birth rapidly moved out of major
airways & replaced by air during 1st few breaths at
birth requiring more force than subsequent
breaths
Initiation of 1st breath is spontaneous & result of
dec. 02, inc. C02 in infants blood & cutaneous
stimulation associated w/ birth process

LUNG GROWTH
Lungs grow fairly rapidly after birth
Lungs larger in boys than girls esp after 2 y/o
Growth stops at 17.9 yrs in girls & 19.8 yrs in
boys
Lung continues to grow at least 1 yr after somatic
growth has stopped
Most of growth of thorax is in height
Basic unit of lung: acinus
The lung segment beyond terminal bronchiole
Area of lung where gas exchange occurs

 Rapid alveolar multiplication: 1st 2 yrs of life

Approximate # of adult alveoli reached at 8 y/o
True alveoli present at birth (?)
Parts of NBs lung exchange gas & act like alveoli

Reticular && elastic fibers in NB lung LOW

Lung structure is weak in NB

RR in NB: 40-60/min
5y/o: 20-30/min

SURFACE FORCES
Surface tension depends on having air-liquid
interface
Fluid initially present in airway affects the ability of
lung to be inflated
Amniotic fluid has more resistance to movement
than lung liquid
Lung liquid w/ surfactant has the lowest
resistance
Little or no surfactant: inc. tendency for lung
collapse
Surfactant diminishes surface forces & dec. the
tendency of lung to collapse

Importance of surfactant
Stabilizes the lung & allow an air volume known
as FRC to be present at expiration
Provides for a more compliant lung
Easier to inflate

Keep excess fluid out of the air spaces in the lung

Inc. in surfactant up to 34 wks AOG ffd by sharp
inc. at 35 wks
Premature infant
Diminished surfactant
Noxious stimuli (asphyxia, acidosis) at birth RDS
Glucocorticoids to mother before birth (+) surfactant
production to dec. risk of RDS among PT

Summary.
Surfactant: synthesized by type II alveolar cells
Forms a surface film that allow lungs to retain
residual air, inc. compliance, helps remove alveolar
fluid

Appears 1st at 24wks AOG

MECHANICS OF VENTILATION
Inspiration
Diaphragm contracts
Abdominal content descend & move forward
Inc. chest cavity
Enlargement of rib cage (minimal)
Infants/children: chest appears to sink in during
inspiration
Paralyzed hemidiaphragm: (esp during birth)
Paralyzed side will move in opposite direction or
upward during inspiration
Accessory muscles of inspiration used when inc.
breathing is needed
Ext. intercostal muscles: life ribs for chest expansion

 Strenuous breathing:
Accessory muscles lift sternum & elevate 1st 2 ribs
Alar flaring

Expiration passive
w/ relaxation after inspiration lung & chest wall
returns to resting position air leaves chest
Active phase of expiration
Int. intercostal muscles dec. chest diameter,
diaphragm pushed upward
Newborn: expiration interrupted before relaxation
volume, protecting FRC

Pressure-volume relationships
Hysteresis
Difference bet. Inspiration & expiration

Resting position: there is still some gas in lung

When lung is w/in chest, resting gas volume is
greater bec. Lung is held more inflated by position
of chest wall
Pleural space filled w/ small amount of fluid
Represents a potential space
When atmospheric pressure is introduced into pleural
space, lung collapses inward, chest wall moves
slightly upward

Compliance
Ease at which it is deformed or distended
Volume change per unit of pressure
Adult lung has greater compliance than infant lung
Specific compliance: comparing compliance w/
specific unit of lung volume (FRC)
Reduced when:

Pulmonary vessels engorged w/ blood

Stiff lung due to inflammatory process
Pulmonary edema
Atelectasis - parts of lung have collapsed

Older child: compliance is frequency dependent

Decreasing w/ inc. frequency

Compliance
Classic method for measuring lung compliance
has been to measure Transpulmonary pressure
that distends the lung by comparing intrapleural
pressure w/ airway pressure & determine
consequent volume change
Methods in measuring static lung compliance
Interrupt flow at various levels of expiration &
measuring pressure at equilibration
Infants: use anesthesia, positive pressure &
relaxation w/ muscle paralyzing agents
Utilize Hering-Breuer Reflex

 Volume measurement
Use Pneumotachograph: measure flow & volume
Problems: nasal prongs or mask interfere w/
breathing pattern
Use of esophageal balloon not advisable among
prematures

Respiratory inductance plethysmograph

NB compliance
4-6 ml/cmH20, FRC 17ml/kg

Pneumotachograph

Pletysmograph

Resistance
lung expansion opposed by forces from elasticity
of lung & resistance to the movement of air
Elastic forces that tend to collapse lung is present
whether there is movement or not at any stage of
expansion
Airway resistance is present only when there is
movement of air
Less with laminar flow, inc. w/ turbulent flow
Depends primarily on diameter of air passages
Major resistance to air flow in the lung: large air
passages

 Newborns: nose breather

Partial obstruction of nose may significantly inc. work
of breathing
Complete obstruction may be lethal

Resistance dec. with inc. lung & airway size

Inc. w/ low lung volumes
If lung volume is exceedingly low, small airways at
bottom of lung will collapse atelectasis of
dependent areas of lung
Contraction of bronchial smooth muscle will also
narrow airways, inc. airway resistance

TIME CONSTANTS
A measure of how fast the lung or individual lung
unit will empty or fill
Expiratory time constant
Compliance x Resistance

Rapid ventilation
Not enough time to empty the lungs inc. lung
volume & inadvertent positive end-expiratory
pressure if mechanical ventilator is used improve
02 from inc. mean airway pressure w/ reduced
ventilation

Work of Breathing
Rate of breathing is regulated to produce
maximum efficiency & minimize work of breathing
Patients w/ reduced compliance: small, rapid
breaths
Airway obstruction: breathing rate is slower
Respiratory muscle fatigue can occur when work
of breathing is high

VENTILATION
LUNG VOLUMES
Tidal Volume: Volume moved w/ inspiration or
expiration during quiet breathing
Maximum inspiration inc. lung volume to max.
inspiratory level
Max. expiration dec. lung volume down to residual
volume
Vital Capacity:volume bet. Max. inspiration &
maximum expiration
FRC (functional residual capacity : Volume remaining
at resting expiration

 Tidal volume, maximum inspiration, maximum

expiration easily measured w/ spirometer
FRC, residual volume,total lung capacity measured
w/ whole body pletysmograph

Each inspiration is composed of gas that reaches

alveoli & gas that only fills the non-gas
exchangeable part of lung
Total ventilation = Vo ventilation (anatomic dead
space) + Va (alveolar ventilation)
Ventilation has direct effect on pC02

VENTILATION-PERFUSION
RELATIONSHIPS (V/Q)
Neither ventilation nor perfusion is uniform
throughout lung
Ventilation & perfusion better in lower parts of
lung
Bec. Of inc. hydrostatic pressure

Low V/Q ratio is one of causes of hypoxemia

Other causes of hypoxemia
Hypoventilation - dec. 02, inc. C02
Diffusion problems diseased lung
Shunting greater in NB due to FO or DA that may
remain open
RDS, cyanotic CHD

DIFFUSION
Movement of 02 from alveolus to blood, C02 from
blood to alveolus (passive process)
P02 in atm: 105mmHg ; venous p02: 40mmHg
02 moves rapidly into the blood

Inc. cardiac output (exercise) reduce the transit

time of blood through lungs
High altitude: inspired 02 is less, much smaller
gradient problems in getting enough 02 into
the blood
Diffusion of gas directly proportional to area
where diffusion occurs & inversely proportional to
thickness of diffusion medium

BLOOD TRANPORT OF 02 & C02

02 transported as dissolved
02 bound to hemoglobin
Majority of 02 carried in
combination w/ hgb
Factors that affect
dissociation curve

pH, pC02, temperature, 2-3

DPG
Shift to right: inc. pC02, temp
or 2-3DPG, dec. in pH

02 dissociation curve

plots the proportion of hemoglobin in its

saturated form on the vertical axis against the
prevailing oxygen tension on the horizontal
axis. The oxyhemoglobin dissociation curve is
an important tool for understanding how our
blood carries and releases oxygen

 C02 transported in dissolved & combined form

More soluble than 02
Majority carried as HC03
Carbonic anhydrase in rbc facilitates formation of
carbonic acid by hydrating C02 HC02
Also transported bound to carbamino groups of hgb
molecule

Bohr Effect :
At tissue level, when there is high C02 & dec. 02,
high C02 aids in unloading 02

Haldane Effect
Dec. P02 aids in loading C02

Inc. p02 aids in unloading C02, dec. pC02 inc.

loading capacity of 02

Control of breathing
Main center for ventilation: CNS (medulla & pons)
Medulla: rhythmic center for breathing
Pons & medulla act together to modulate smooth
transition from inspiration to expiration
Modified in involuntary breathing or breath holding

Newborn: chest wall is compliant

FRC maintained by breaking of some inspiratory
muscles during expiration

Many signals come to CNS via vagus nerve

Receptors: peripheral chemoreceptors, central
chemoreceptors, lung receptors

 Peripheral chemoreceptors: carotid & aortic

Respond primarily to 02
Carotid body: junction of common carotid artery
Aortic body: arch of aorta
Drop in p02 inc ventilation
Primary response triggered by acute hypoxia
No role in changes that occur during exercise but
provide some response to changes in pH & PC02

Central chemoreceptors: respond to changes in

H+ & pC02 located in CNS near medulla in 4th
ventricel
Shift in C02 concentration controls ventilation but H+
at cellular level is perceived

 Lung receptors
Pulmonary stretch receptors
Discharged during lung distension afferent
impulses to vagus nerve responsible for HeringBreuer reflex (slowing of respiratory frequency
due to inc. of expiratory time

Irritant receptors: causes bronchoconstriction &

hyperpnea
Response to changes in C02 concentration is
rapid & large compared to changes in 02 & pH
No response to changes in 02 concentration until
alveolar p02 falls <50mmHg

Chronic lung disease

Blunted response to C02 hypoxic response
Drop in pH inc. ventilation

Antenatal Assessment and High-Risk

Delivery

Fetal and Newborn Assessment

in the L and D

Objectives
At the completion of this lecture the student will:
Be able to discuss relevant points concerning
Antenatal Assessment
Be able to ID the L and D cases which may
present a high-risk delivery
Know the parameters on which to base
antenatal/perinatal assessments

Evaluation of Neonatal Patient

Respiratory distress: 1st symptom of group of
conditions that account for neonatal mortality &
morbidity

Antenatal Assessment and

High- Risk Delivery
Indications of a High-Risk Delivery:
Incompetent Cervix
Toxic habits in Pregnancy
Hypertension and Diabetes Mellitus
Preclampsia
Severe Preclampsia
Infectious Disease
Multiple birth

Antenatal Assessment and

High- Risk Delivery
Indications of a High-Risk Delivery:
Long cord, Nuchal cord, cord knots
Placenta Abruption
Placenta Previa
Disorders of aminiotic fluid
Abnormalities of Umbilical cord
Oligohydraminos, Polyhydraminos

Antenatal Assessment
Antenatal = Around birth time, usually
considered prior to L and D

Ultrasound
Amniocentesis
Shake test
Fetal Biophysical profile
Preterm Pregnancy
Less than 37 weeks

Indications of High-Risk
Delivery
Magnesium sulfate is given to stop contractions
Blood gas with Ph less than 7.15 can be an
indication of asphyxia
Post-term Labor
Pregnancy continued beyond 42 weeks
Pre-term less than 33 weeks ges age
Lack of prenatal care

Neonatal Assessment and

Resuscitation
Neonatal Resuscitation Considerations While
Assessing the Patient
Maintain warmth
Cold stress increases oxygen consumption
Maintain an airway
Placing a small roll under the shoulders will
correct the position
Suction the airway
Stimulation
Obtain vascular access
Provide resuscitative drugs PRN

Assessing the Neonate

Vital signs
Apgar score
Neonatal resuscitation
When is Positive pressure ventilation Indicated?
When is Intubation Indicated?
When are chest compressions indicated?
When are Medications indicated?

Resuscitation of New Born

Supportive
Supportive
Care
Care

Routine
Routine Care
Care
Provide
Provide warmth
warmth
Clear
Clear Airway
Airway
Dry
Dry

Breathing
HR >100
Pink

Yes

Birth
Birth

Clear
Clear of
of Meconium?
Meconium?
Breathing
Breathing or
or Crying?
Crying?
Good
Good Muscle
Muscle Tone?
Tone?
Color
Color Pink
Pink ??
Term
Term gestation?
gestation?

Approximate Time
30 sec

Provide
Provide warmth
warmth
Position
Position
Clear
Clear Airway
Airway
(as necessary)
necessary)
NO (as
Dry,
Dry, stimulate
stimulate
Reposition,
Reposition,
Give
Give O
O22

Ongoing
Ongoing care
care

Ventilating
HR >100
Pink

Evaluate:
Evaluate:
Respirations
Respirations
Heart
Heart rate
rate
Color
Color

PPV
PPV

Apnea or
HR<100
30 sec

HR < 60

PPV
Chest Compressions

Administer
Epinephrine
HR <60

HR >60
Time
30 sec

Assessment of Neonatal
Patient
Vital signs
Skin
Mottling
Irregular areas of dusky skin alternating with pale
skin
Capillary refill

Respiratory Function
Assessment

Apnea
Periodic breathing
Grunting
Nasal flaring
Retractions
Silverman score
Stridor
X-ray

Nasal Flaring and Sub-sternal

Retractions

Nasal Flaring and Substernal

Retractions

Silverman score

Cardiac Assessment
Heart, how is it working?
HR, RR,BP
Cardiac murmur PDA
Weak pulse Coarctation of Aorta
Hypo plastic Left heart syndrome
Adequate MBP= gestational age + 5

Abdomen

Diaphramatic hernia
Omphalocele
Gastroschisis
Umblical cord
A single umblical artery
Congenital anomalies
Thin cord
Thick cord-diabetics

Head and Neck Assessment

Microstomia-small mouth
Micrognathia-small jaw
T-E fistula
Pierre robin syndrome
Choanal Artesia
Macroglossia

Assess an Infants Cry

Loud and vigorous- healthy infant

Grunting cry- RDS
Hoarse cry-laryngeal edema
Cat like cry- chromosme abnormality
High-pitched cry- neurological deficit

Pediatric Assessment
Pedi assessment is focused on different indications:
History and assessment
Chief complaint
Medical history
Family history
Environmental history

Elements of Pediatric Physical

Assessment

Assessment
Inspection
RR
Retractions
AP diameter
Digital clubbing
Palpation
Tactile fremitus
Position of trachea
Percussion
Auscultation