FETAL CIRCULATION
aorta flows all the way around aortic arch to the
R nd L ventricles: parallel circuit
Placenta gas and metabolite exchange
therefore pulmonary vessels are
vasoconstricted, diverting blood away from
the pulmonary circulation;
NOTE: 3 cv structures unique: ductus venosus
and arteriosus, foramen ovale
Umbilical venous PO2 = 30-35 mmHg
(mababa)
50% umbilical venous blood -> hepatic
circulation
other 50% -> liver -> INF. Vena cava (via
ductus venosus)
INF VENA CAVA BLOOD
at INF. Vena cava, blood mixes with POORLY
oxygenated inf vena cava blood na
nanggaling sa lower part of the fetal body
the mixed blood then enters RIGHT ATRIUM
and directed by a flap of tissue at right
atrial-inf vena caval junction, the eustachian
valve, across foramen ovale to the L atrium
(MAJOR SOURCE OF L VENTRICULAR BLOOD
cause pulmonary venous return is minimal)
L ventricular blood ejected ASCENDING
AORTA (supplies upper body and brain)
SUP VENA CAVA BLOOD
-less oxygenated
Blood -> RIGHT ATRIUM -> flow across
tricuspid valve (not foramen ovale) to go
to RIGHT VENTRICLE
Blood from R.V. ejected pulmonary
artery (vasoconstricted so 5% lang
pupuntang lungs)
Lungs -> flows right-to-left via ductus
arteriosus -> descending aorta (to
perfuse lower part of the fetal body)
*Upper part of the detal body is perfused
exclusively from LV with higher P02 than blood sa
lower part which is derived from RV
*Only small volume of blood from ASCENDING
descending aorta
TOTAL FETAL CARDIAC OUTPUT = 450 mL/kg/min
65% descending aortic blood flow returns to
placenta; 35% perfuses the fetal organs and
tissues
RV output is 1.3 times LV flow. Therefore,
during fetal life, RV is performing a greater
volume of work than LV
In narrowing of an upstream structure, LV
growth maybe compromised (hypoplastic
left heart syndrome)
Treatment: opening narrowed aortic valves
in mid-gestation fetuses allowing more
normal LV growth
TRANSITIONAL CIRCULATION
At birth
- Mechanical expansion of lungs and increase
in arterial PO2 -> rapid DECREASE in
pulmonary vascular resistance
- Removal of low-resistance placental
circulation -. INCREASE in systemic vascular
resistance
- RV output flows entirely into pulmonary
circulation so since pulmonary vascular
resistance ay mas mababa kaysa sa systemic
vascular resistance, shunt through ductus
arteriosus reverses and becomes L to R.
- Several days after, HIGH arterial PO2
constricts -> closes ductus arteriosus so
magiging ligamentum arteriosum
- INCREASED volume of pulmonary blood
blow na bumabalik sa L atrium from lungs =
INCREASES L atrial volume and pressure so
mag c-close yung flap ng foramen ovale
altho pwede magremain probe patent
-
- Removal of placenta -> closure of ductus
venosus so LV now coupled to high-
resistance systemic circulation tapos lalapad
na wall and tataas mass
- In contrast, RV coupled to low-resistance
pulmonary circulation
 - LV must now deliver the entire systemic
cardiac output (hormonal and metabolic
signals like increase in catecholamines)
- S
- When ductus arteriosus and foramen ovale
dont close completely at birth, remains
patent in certain congenital cardiac lesions
- Therapeutic agents: prostaglandin E1
(maintains fetal pathways); indomethacin
(hasten their closure)
NEONATAL CIRCULATION
- At birth, mag adapt dapat agad na lungs na
as gas exchange; mag d-DECREASE yung
pulmonary vascular resistance dahil sa both
active and passive pulmonary vasodilation
- In normal neonate, closure of ductus
arteriosus and fall in pulmonary vascular
resistance DECREASES pulmonary arterial
and right ventricular pressuers
- Over next several weeks of life, pulmonary
vascular resistance decreases even further;
remodeling of pulmonary vasculature
(thinning of acscular smooth muscle and
recruitment of new vessels)
- As pulmonary resistance decreases in the
next week or 2, volume of left-to-right shunt
through ventricular septal defect increases
-> symptoms of heart failure within the 1st
month or 2 of life
DIFFERENCE NG NEONATAL AND INFANT
CIRTULATION
Right-to-left or l2r shunting may persist
across the patent foramen ovale
In presence of cardio-pulmonary disease,
continued patency of the ductus arteriosus
may allow l2r,r2l or bidirectional shunting
Neonatal pulmonary vasculature constricts
stronger in response to hypoxemia,
hypercapnia and acidosis
Wall thickness and muscle mass of neonatal
L and R ventricles are almost equal
Newborn infants at rest have relatively high
oxygen consumption so high cardiac output
- Newborn cardiac output (1-2 months): 150
ml/kg/min then magiging 75 nalang
- Altho HgbF is beneficial to delivery of O2 in
low PO@ fetal circulation, high percentage of
HgbF in newborn may actually INTERFERE
with delivery of O2 to tissues in high
systemic PO2 neonatal circulation
- K
- Foramen uvale: closed by 3 mos of life pero
possible parin magpass sa probe via
overlapping flaps in a large % of children
and in 15-25% adults
- Functional closure of ductus arteriosus:
complete by 10-15 hour in a normal neonat
pero may remain patent much longer in the
presence of congenital heart disease esp.
pag associated sa cyanosis
- In premature newborn infants, short-life
systolic murmur with late emphasis or
continuous murmur may be audible
- A
- Normal ductus arteriosus mas maraming
circularly arranged smooth ms in medial
layer kaysa sa adjoining aorta and
pulmonary artery
- During fetal life, patency (clearness) of
ductus arteriosus appears to be maintained
by combined relaxant effects of LOW O2
tension and endogenously produced
prostaglandin E2
- In a full-term neonate, O2 is the most
important factor controlling ductal closure
- When PO2 of blood na nagpapass sa ductus
ay 50 mmHg, ductal wall begins to
CONSTRICT so effects of O@ on ductal
smooth ms may be direct or mediated by its
effects on prostaglandin synthesis
- Ductus of premature infant: less responsive
to O2 kahit na nadevelop na musculature