Physiology of transition period in a neonate with regard to Respiratory System and administration of Anesthesia in such a circumstance

1. PHYSIOLOGY OF TRANSITION PERIOD
IN NEONATES WITH RESPECT
TO RESPIRATORY SYSTEM
Speaker: Dr Bhagirath.S.N
Moderator: Dr Sarika

2. Prenatal development of the lungs

3. Some concepts….
Surface Tension
Property of the surface of a liquid that allows it to resist an external force. (by virtue
of cohesive forces between its molecules)
What exactly does surfactant do..?
It forms a monolayer that adheres closely to the alveolar interface and prevents
the sac from collapsing once the fluid is removed..
How then is the fluid removed..?
Most of it is expelled by the upper airways.
Rest of it is drained by the lymphatics and capillaries.
What provides the force required to force open the partially
collapsed fluid filled alveolar sacs..?
A negative intrathoracic pressure of -30 to -70 cms of H2O that is created by the
first gasp of air.
What induces this gasp of air..?
Clamping of the cord asphyxiates the baby provoking a violent gasp of air.

4. Some concepts….(continued)
So, does this first gasp of air represent the first breath…?
• Boddy & Robinson ((1971) were among the first to demonstrate foetal breathing
in-utero.
• Patrick et al (1980) demonstrated the presence of fetal breathing >30% of the
time in utero and further recorded a increase in movements subsequent to a
maternal meal.
• Motoyama demonstrated a increase in FRC on inducing hypercapnia in the fetus.
So, the traditional concept that the first gasp represents the first breath now stands
challenged.
Why does the fetus need to breathe when the placenta is breathing for it..?
• Unclear. But thought to be as a prenatal practice for postnatal life and probably to
act as a stimulus for lung development…

5. Respiratory rate
O2 consumption is neonates is double that of an adult
Minute ventilation is very high
Minute ventilation is the product of respiratory rate and tidal volume
Since tidal volume is almost same as a child/adult on a volume/Kg/body weight
measure, the only factor that can be augmented is the rate.
This explains why the respiratory rate is so high in a neonate.
Analogous to increasing heart rate to compensate for the fixed stroke volume, so that
on the whole cardiac output remains maintained.

6. Respiratory reserve
Lung volume of the neonate is disproportionately small in relation to body size
Further complicated by the increased metabolic rate (O2 consumption/unit body
weight being twice as that of adults)
i.e. the respiratory reserve is less
This calls for increased ventilatory requirements.
Relative to the increased ventilatory requirements the lung surface area available
for gas exchange is less
Primary reason why neonates become rapidly desaturated with hypoventilation or
apnea of relatively short duration
Implication

7. Compliance-ability of the lungs & thorax to expand
To not react is to be compliant; To react is to be less compliant;
What determines the recoiling nature of the lung & the chest wall..?
Elastic fibers in the lung tissue, elastic rib cage architecture, good diaphragmatic
effort all of which are either deficient or immature in the neonate.
Neonatal
lung
Adult
lung

8. Compliance …(contd)
Neonates have a high compliance because:
• Poorly developed intercostal muscles
• Pliable rib cage (cartilaginous)
• Poor diaphragmatic effort due to abundance of type 2 fast twitch, low oxidative
fibers that contract in quick succession but invariably fatigue early.
Anaesthetic implication
• Under general anesthesia the neonatal lungs are more prone to collapse as
skeletal muscle relaxation ensues around the chest wall, what precious little
rigidity that prevented the collapse is now lost.

9. Surfactant
• Secreted by type 2 pneumocytes
• Chemically: dipalmitoylphosphatidylcholine
• maintains distensibility of alveoli by reducing surface tension
• Laplace law: The gas pressure (P) needed to keep equilibrium between the
collapsing force of surface tension (γ) and the expanding force of gas in an
alveolus of radius r is expressed as P = 2 γ/r
• decreased levels are seen in premature babies and babies born to diabetic
mothers
• decreased levels predispose to respiratory distress syndrome (RDS) , which
includes:
1. Alveolar collapse
2. Decreased compliance
3. Hypoxia
4. Increased work of breathing
5. Ultimately respiratory failure.

10. Control of breathing
• The respiratory centers are still immature and are unable to control breathing
effectively.
• Neonatal response to hypercapnia is less compared to a child but none the
less is mounted in the form of hyperventilation albeit for short durations.
• Under conditions of hypothermia, initial hyperventilatory response may be
blunted.
• Periodic breathing
 breathing is interposed with repetitive short apneic spells lasting 5 to 10
seconds without haemoglobin desaturation or cyanosis
 Seen in both REM and NREM sleep.
 thought to be due to changes in respiratory mechanics rather than reduced
sensitivity to CO2

11. Control of breathing….(Contd.)
•Apnea of prematurity & hypoxia
 unexplained cessation of breathing for 15 seconds or longer or a shorter
respiratory pause associated with bradycardia (heart rate <100), cyanosis, or
pallor
 may be related to an immature respiratory control mechanism
 thought to be due to changes in respiratory mechanics rather than reduced
sensitivity to CO2

12. Persistent pulmonary hypertension of newborn
• Collapsed fluid filled alveoli, collapsed capillaries and decreased perfusion offer
resistance to flow of blood through pulmonary vasculature in utero
• i.e. pulmonary vascular resistance is high in utero
• If the same resistance due to any reason is encountered in the post natal
period, then the pressure in the pulmonary artery is elevated to overcome such
resistance.
• i.e. pulmonary artery hypertension ensues..
Precipitating factors include:
1. Hypoxia
2. Preterm
3. Birth asphyxia
4. Meconium aspiration
5. Sepsis
6. Congenital diaphragmatic hernia
7. Maternal use of NSAIDs.

13. Persistent pulmonary hypertension of newborn….(Contd)
Other risk factors include:
1. Maternal diabetes
2. Asthma
3. Caesarean delivery
Increased pulmonary artery pressure
Increased right ventricular pressure
Increased right atrial pressure
Throws open the foramen ovale
Blood reaches the aorta
as pulmonary artery pressure is
Ductus arteriosus is thrown open
Hypoxia & normal to elevated
PaCO2
• Treatment
Increase tissue oxygenation
Target PaO2 -50-70 mm of Hg
Mechanical ventilation
High frequency ventilation
Exogenous surfactant
Alkalinisation
ECMO
Sildenafil

14. Persistent pulmonary hypertension of newborn….(Contd)
•Meconium aspiration
 this is different from meconium aspiration at labour
This happens in utero.
Seen when the fetus has been exposed to prolonged periods of hypoxia
Can predispose to persistent pulmonary hypertension of newborn.

15. References….
Ganong’s review of physiology
23rd edition
P582, 584
Guyton & Hall’s Text book of Physiology
11th edition
P1022, 1023

16. References….
Clinical Anesthesia by Paul.G.Barash
6th edition
P1127, 1129
Miller’s Anesthesia
7th Edition, Vol 1
P889. 890

17. References….
Physiology for anesthetists
Wolters Kluwer
Chapter 4
Smith’s anesthesia for infants and
children
Motoyama and Davis
Chapter 6