The document summarizes key aspects of fetal, neonatal, and infant physiology relevant to anesthesia and surgery. It describes the fetal circulation, how the lungs are bypassed, and drug transfer across the placenta. After birth, changes include closure of openings between heart chambers, increased pulmonary blood flow, and transition to adult circulation. The neonatal respiratory, cardiovascular, temperature regulation and renal systems have limited capacity due to immaturity. Care during anesthesia and surgery must account for these physiological differences.

1. NEONATAL AND
FETAL
PHYSIOLOGY
BY: SHEENA SHARMA

2. Characteristics of fetal circulation
• The fetal (prenatal) circulation works differently from normal
postnatal circulation, mainly because the lungs are not in use. Instead,
the fetus obtains oxygen and nutrients from the mother through
the placenta and the umbilical cord.[1] The blood flow through the umbilical cord is
approximately 35 mL/min at 20 weeks, and 240 mL/min at 40 weeks of gestation.[8] Adapted to
the weight of the fetus, this corresponds to 115 mL/min/kg at 20 weeks and 64 mL/min/kg at 40

3. • Blood from the placenta is carried to the fetus by the umbilical
vein. less than a third of this enters the fetal ductus venosus and
is carried to the inferior vena cava,[2]
while the rest enters the liver,
The branch of the umbilical vein that supplies the right lobe of
the liver first joins with the portal vein. The blood then moves to
the right atrium of the heart. In the fetus, there is an opening
between the right and left atrium (the foramen ovale), and most of
the blood flows through this hole directly into the left atrium from
the right atrium, thus bypassing pulmonary circulation. The
continuation of this blood flow is into the left ventricle, and from
there it is pumped through the aortainto the body. Some of the
blood moves from the aorta through the internal iliac arteries to
the umbilical arteries, and re-enters the placenta, where carbon
dioxide and other waste products from the fetus are taken up and
[

5. The fetal circulation is characterised by
: high pulmonary vascular resisatance,low
systemic vascular resistance and rt to left
cardiac shunting via the foramen ovale and
ductus arteriosus.

6. Drug Metabolism and liver functions
• Drug transfer of less thn 1000 Dalton occurs primarily
by diffusion. The rate of diffusion depends on :
maternal to foetal concentration gradients{mainly},
maternal protein binding,molecular weight of sub, lipid
solubility and degree of ionization.
Eg.heparin, glycopyrolate,succinylcholine are ionized and
are not transferred.
Whereas volatile agents, benzodiazipines,local
anesthetics,and opioids transfer is facilitated by:low

7. •
•
ION TRAPPING: Foetal blood is more acidic thn maternal
blood and the lower ph creates an environmt where weakly
basic drugs lyk local anesthetics can cross placenta and
thn becom ionized in fetal circulation.this drug now has
resistance to diffusion back across placenta, the drug
accumulates in fetal circulation and reaches level higher
tthan maternal blood.
High conc. Of local anesthetics in fetal circulation
decreases neonatal neuromuscular tone.resulting in variety
of effects lyk bradycardia, ventricular arrhythmias,
acidosis, and severe cardiac depression.

8. • The anatomy of foetal circulation helps to decrease
fetal exposure to potentially high conc of drugs in
umblical vein, approx. 75% of blood initialy passes
through the foetal liver leading to significant drug
metabolism although enzyme activity is less developed,
secondly drug entering the inferior vena cava via ductus
venosus is initaly diluted by drug free blood returning
from the fetal lower extremities and pelvic viscera of
fetus.

9. • Liver functions: coagulation factors are synthesised
independent of maternal circulation,thy do not cross
placenta and their conc increases with gestational age.
However clot formation is less robust in comparison to
adults.

10. Anesthetic toxicity in fetus
•
•
All general anesthetic drugs cross the placenta.while there
is no clear evidence for toxicity of specific anesthetic
drugs in humans.
Studies have found an excess of birth defects in women
who underwent general anesthesia during pregnancy. In
general the second trimester is preferrd for surgical
interventions as this is a period after organogenesis and
minimizes the risk of preterm labor associated with third
trimester .

11. Fetal neurophysiology
•
•
Although functional circuitary required for sensation of
pain is likely to be present between 20 -30 weeks of
gestation,but the experience of pain requires
a)nociception b) perception with emotional response.
Nociception fibres come by 20 th week of gestation but
second requirement of perception with emotional
response is difficult to establish.

12. Neonatal physiology
•
•
•
•
In neonatal physiology ,the changed which take place
include:
Limited reserve capacity for cardiovascular,respiratory
and temperature control
Variables and individualized fluid requirement
Implications of hepatic and renal immaturity.

13. NEONATAL CVS
•
•
The newborn infant is in a state of transition from the
fetal intrauterine to the newborn extrauterine
circulation.Expansion of lungs at birth increases Po2
and causes a rapid decline in pulmonary vascular
resistance caused via action of endogenous nitric oxide .
This leads to increase blood return to heart ,causing
increase in left atrial pressure causing functional
closure of foramen ovale.
Although anatomical closure occurs between 3months

14. •
•
Clinical fact: In most of the individuals with
anatomicaly patent foramen ovale “probe patent”,
foramen is functionaly closed by lack of any
significant pressure gradient ; in conditions where
pulmonary vascular resistance rises, significant rt to
left shunt can occur. Individuals with probe patent
foramen are also at risk of systemivc air embolism and
resultant stroke whn air emboli passes from pulmonary
to syatemic circulation.
Also as the foramen and DA are only functionaly closed

16. •
•
•
•
•
R-L SHUNT
HYPOXEMIA
INCREASED Pulmonary vascular
resistance
DECREASED FLOW TO LEFT SIDE
Persistent pulmonary hypertension may be seen in neonates
and also in those with MAS,congenital heart disease,

17. •
•
•
Neonatal myocardium:
immature contractile elements: less compliant: stroke volume cannot
be increased more. Frank Starling relationship is functional only
within a very narrow range of left ventricular EDP, (CO= SV X HR ) (
SV= EDV-ESV).To meet elevated demand neonatal CO is twice tht of
adult. This is achieved by a relatively rapid heart rate (140 bpm).
Clinical fact: hence less(limited) increase in cardiac output from
aggressive volume overloading in normovolemic neonates.but not in
case of hypovolemic or dehydrated neonates.

18. •
•
Neonatal circulation is characterised by by
CENTRALIZATION i.e. increased PVR and distribution
of CO primarily to vital organs.
Neonatal baroreflex activity is impaired , the response
to hemorrahge produces littles increase in heart rate ,
thus evn 10%reduction in blood vlume will cause a
15-30% decrease in mean blood pressure.

19. NEONATAL RESPIRATION

22. •
•
Fewer high oxidative muscle fibres in diaphragm and is
thus less fatigue resistant than in adults. V/Q
imbalance occurs as a result of distal airway closure
during normal tidal breathing in neonates.
This phenomena is responsible for an increase in
alveolar-arterial oxygen tension gradient compared to
adults.

24. •
•
•
•
The neonatal chest wall is more compliant and has less
outward recoil thn tht of adults. Thus neonatal lung
has a greater tendency to collapse and the infant is
obliged to utilize active mechanisms to maintain
normal lung volumes :
Rapid respiratory rate-early termination of expiration
Intercoastal muscle activity in expiration –stabilizes
compliant chest wall

25. Alveolar minute ventilation(RR X TV) =2 X adults ( to fulfil
increased oxygrn demand)

26. •
•
•
Since neonatal alveolar ventilation is twice tht of an adult, the
ratio of alveolar ventilation to FRC in neonates is x 2 tht of an
adult.
The high ratio of minute ventilation to FRC causes a more rapid
wash out or wash in of oxygen and anesthetic drugs in response to
change in inspired concentrations.
The active mechanisms utilized by newborn to protect lung
volumes are exquisitively sensitive to effects of general
anesthesia . Therefore the neonatal FRC may decrease
significantly during anesthesia particularly during periodic
breathing and apnea.

27. •
•
Peripheral chemoreceptors: active from 28th
week of
gestation, but their function is immature yntill several
days after birth. Hence neonatal preterm infants
exhibit an altered response to hypoxia and hypercarbia.
These impaired responses are contributing factors to
the development of life threatening apnea and
htpoventilation .

28. NEONATAL THERMOREGULATION

31. During anesthesia and surgery:
• Other factors are: decrease in thermoregulatory threshold
due to anesthesia, low ambient temperature of operation
theatres, preparation of skin with cold solutions, infusion
of cold solutions, anesthesia induced vasodilatation, and
use of dry anesthetic gases in high flow, non rebreathing
systems.

32. •
•
•
•
INTRAOPERATIVE HYPOTHERMIA WILL :
Markedly delay emergence
With return of thermostatic reflexes, oxygen consumption
increases by 3-4 fold as metabolic rate is increased in an
attempt to generate heat.
This additional demand on immature
cardiorespiratory system tht is already compromised due
to residual effect of anesthesia and surgery may ppt
cardiorespiratory failure.

33. • Prevention :using radiant heat lamps, wrapping the
extremeties with insulating material, using non volatile
warmed solutions for skin prepration, administration of
warmed i/v fluids and blood products.

34. NEONATAL FLUID AND RENAL
PHYSIOLOGY

36. • Neonates are obligate sodium wasters and require
sodium supplementation. All theses factors contribute
to potential for overhydration, dehydration, metabolic
acidosis, and hyponatremis necessitating meticulous
attention to intraoperative fluid therapy.

38. NEONATAL NEUROPHYSIOLOGY

40. • The concept of plasticity of nervous system has
important implications for the management of pain
newborns. The failure to provide analgesia for neonates
leads to changes in nociceptive pathways in dorsal horn
of spinal cord and in the brain .As a result future painful
insults result in exaggerated pain perception .

41. • NON PHARMACOLOGICAL METHODS: Analgesia may
be induced by administration of sucrose and by
suckling .these effects are mediated via descending
endogenous opioid and non opioid mechanisims
originating in brainstem.