7. SHUNT THROUGH DV
ā¢ Shunting more prominent before 30 weeks of gestation.
ā¢ During the last 8 to 10 weeks of pregnancy 80% of the umbilical blood perfuses the liver,
signifying a very high developmental priority of the umbilical liver perfusion compared with
the ductus venosus.
ā¢ During hypoxic challenges, priority - different. Fetuses maintain a higher degree of ductus
venosus shunting,(redistributional adaptation), ensuring oxygenation of the heart and brain.
8. DOPPLER EXAMINATION OF DV-
ā¢ identify hypoxaemia, acidosis, cardiac decompensation and placental compromise.
ā¢ Promising tool for timing the delivery of critically ill fetuses.
ā¢ Increased pulsatility, mainly caused by the augmented atrial contraction wave, signifies
increased atrial contraction due to adrenergic drive, or increased venous filling pressure, or
both.
ā¢ In early pregnancy, the augmented a-wave in the ductus venosus - increased risk of
chromosomal aberration secondary screening test
10. UMBILICAL BLOOD FLOW TO THE
LIVER AND METABOLIC FUNCTION
ā¢ Translate transplacental information into differential growth and adaptive development.
ā¢ Increasing umbilical blood flow into the fetal lamb liver induced liver cell proliferation and
increased production of insulin-like growth factor-I and -II, resulting in organ growth in the
fetal body.
11. ā¢ Autoregulation -slim mothers - fetal liver tended to take a larger share of the umbilical flow -
further augmented if the motherās diet was of poor quality.
ā¢ High umbilical flow to the fetal liver resulted in high fat content in the newborn, which was
sustained up to 4 years of age.
ā¢ Development of fetal macrosomia in the absence of maternal hyperglycemia was associated
with increased umbilical flow, particularly during the third trimester
12. ā¢ In growth-restricted fetuses, the liver has a lower priority and more umbilical blood bypasses
the liver to reach the heart and brain directly.
ā¢ This causes a down-regulation of liver growth and enzyme production and reduces hepatic
production of fat, which is much needed for central nervous system development.
13.
14.
15. After birth surge in :-
Catecholamines,
RenināAngiotensin
Vasopressin
Preterm- slower increase in
catecholamine levels
ā¢ Important for the increase in cardiac
output.
ā¢ total cardiac output of 450 mL/kg/min, to
400 mL/kg/min(each ventricle cardiac
output ).
ā¢ Increases in plasma glucose and free fatty
acids
16.
17.
18. PULMONARY ARTERIAL PRESSURE REACHES ONE-HALF THE
SYSTEMIC ARTERIAL PRESSURE BY
24 HOURS OF AGE, ATTAINING ADULT LEVELS BY 2 WEEKS IN MOST
TYPICAL INFANTS
High PVR
Fluid filled lung
Hypoxic vasoconstrictors
Endothelin I
Leucotrienes
Thromboxane
23. RATIONALE FOR DELAYED CORD
CLAMPING
ā¢ Rather than an arbitrary period of time, the infantās respiratory function is likely to be a better
indicator for when the cord should be clamped .
ā¢ That is, waiting until the infant has established effective breathing, particularly if a pulse
oximeter is used and showing an increasing oxygen saturation level, will ensure that PBF has
increased and is able to provide sufficient venous return and preload for the left ventricle.
24. ā¢ Most benefit to those requiring respiratory support immediately after birth.
ā¢ If it is due to cord compression or a placental complication, then it is unlikely that delaying
cord clamping until after ventilation onset will have any benefit.
28. WHAT IS PLACENTOME?
ā¢ Functional unit of the placenta is called a fetal cotyledon or placentome, which is derived from
a major primary stem villus.
ā¢ Functional subunit is called a lobule, which is derived from a tertiary stem villi.
ā¢ Each cotyledon (total 15ā29) contains 3ā4 major stem villi.
ā¢ The villi are the functional unit of the placenta.
30. PLACENTAL CIRCULATION
ā¢ 1) Uteroplacental circulation(maternal)- inter-villous space
ā¢ 2) Fetoplacental circulation
Both circulation run side by side but in opposite direction .
Countercurrent flow facilitates material exchange between the mother and fetus.
34. ā¢ Fetal growth and well-being depend on the development, growth, and maturation of the
placenta, as well as increases in fetal umbilical and maternal placental blood flows.
ā¢ In the last third of pregnancy, fetal and maternal placental blood flows increase
logarithmically, paralleling the increase in fetal weight.
35. ā¢ Maternal placental vasculature is refractory to endogenous and infused vasoconstrictors,
including ANG II and catecholamines, protecting it from the increases and variations in
circulating levels that occur throughout pregnancy.
ā¢ There also is enhanced local synthesis of vasodilators by the uterine and umbilicoplacental
vasculature that not only increase blood flow but may also antagonize vasoconstrictor
responses
36. ā¢ Maternal uteroplacental blood flow normally exceeds fetal-placental metabolic needs,
providing a large āmargin of errorā; thus blood flow may acutely fall by 50% without altering
oxygen and nutrient delivery.
40. DOPPLER VELOCITY WAVEFORMS RECORDED FROM
THE UTERINE ARTERY BEFORE, DURING, AND AFTER
UTERINE CONTRACTION
41. ā¢ Diastolic part of the flow velocity waveform - influenced by the peripheral vascular resistance;
an increase in the resistance lowers the diastolic velocity and, consequently, increases the
values of the waveform indices.
ā¢ In the cerebral vessels of hypoxic fetuses, an increase in diastolic velocity can be observed as
an expression of decreased resistance in the cerebral vascular bed and redistribution of blood
flow (brain-sparing phenomenon
ā¢ A bilateral notch in the uterine artery persisting after 26 weeksā gestation has been shown to
be associated with increased risk of development of preeclampsia and intrauterine growth
restriction