Circulatory Physiology
AnS 536
Spring 2016
Development of the Circulatory
System
1st functional organ system – heart is
functional when embryo is 2 mm in size
 Heart rate peaks at 9 weeks, and slows to
~145 beats at term
 Huge increase in cardiac output
postnatally but limited ability to increase
further

– Increase in thyroid hormone prenatally
matures myocardium in preparation for
increased postnatal requirements
VIDEO BREAK
http://www.youtube.com/watch?v=K4B5fFQ
8OGw&feature=player_detailpage
Development of the Circulatory
System
The heart functions partly in parallel and
dominated by right ventricular function
 Parallel function allows the shunts to be
more effective and the foramen ovale to
not compromise cardiac output
 Heart functions in series postnatally with
equal ventricular function
 Blood volume ~11% in fetus (7.5% in
adults) because of amount of placental
blood

The Fetal Circulatory System: oxygenated blood flow
The Fetal Circulatory System: deoxygenated blood flow
Fetal Circulatory Shunts

Foramen ovale

– Fetal blood passes from the
placenta  umbilical vein  fetal
heart
– Left ventricle shunts blood to the
cranium
– Shunts blood from the
right atrium to the left atrium

Ductus arteriosus
– Shunts blood from the
pulmonary artery to the
ascending aorta
– Bypasses pulmonary
circulation

Ductus venosus
– Shunts blood from the
umbilical vein to the inferior
vena cava
– Separates the hepatoportal
and systemic circulation
Physiology

Advantages of shunts
– Bypasses normal “flow patterns”
to allow most oxygenated blood
(left ventricle) to reach the fetal
brain
– Unsaturated blood (from the right
ventricle) is diverted to the trunk
and lower body of the fetus
Oxygen Tension Levels
Blood coming from the placenta (umbilical veins)
is 80% saturated with oxygen
 Blood enters right atrium via inferior vena cava

– Half of venous return bypasses hepatic portal
circulation via ductus venosus
– Because ductus venosus has small diameter, blood
accelerates and is more likely to push though foramen
ovale into left atrium from right and to “upper
circulation”

From right atrium to left atrium via foramen
ovale (now 65% saturated)
– Pumped to carotid artery and to brain (most oxygen
rich blood)
Oxygen Tension Levels
Blood coming from the superior vena cava is
directed primarily through tricuspid valve into
right ventricle (50% saturated with oxygen)
 Enters aorta, provides lower levels of oxygen to
caudal half of body and then enters the umbilical
arteries to be re-oxygenated in the placenta

– Once oxygenated, returns to body as fully oxygenated
blood via umbilical veins
Ductus Arteriosus

Factors involved in closure
– PGE2 helps maintain patency and nitic oxide
will cause relaxation
– Can induce closure with indomethacin: PGE2
– Increased PO2 of arterial blood postnatally
causes muscular wall constriction
– Fetus has low-resistance circulation from the
placenta during gestation
 Parturition (NE increase) , umbilical cord rupture
(bradykinins), and initiation of respiration increase
resistance
Ductus Arteriosus

Physiological changes
– Lungs become the organ of respiration
– Oxygen tension increases
– Right ventricular outflow passes into the lungs
instead of the ductus
– Ductus constriction begins shortly after birth
– Physical closure occurs ~1 week after birth
– Rise in output from the left ventricle
Ductus Venosus

Factors involved in closure
– Liver pressure and resistance
– Gestational age
and weight at birth
 Premature neonates will have
delayed closure
– Drugs
 Promote closure
– Antenatal corticosteroids
 Delay closure
– Prostaglandins and nitroxide distend
diameter of ductus
Ductus Venosus VIDEO
http://www.youtube.com/watch?v=SUP1K4
gPw4s&feature=player_detailpage
Ductus Venosus

Physiologic changes:
– Ductus venosus becomes ligamentum venosum
– not really functional
– Umbilical vein constricts via bradykinins
– Blood enters liver through hepatic sinuoids
Foramen Ovale

The horizontal diameter between
the foramen ovale valve and the
atrium (broken line) represents
the restricting area into the Left
Atrium

Position, direction and kinetic
energy of the flow from the
ductus venosus makes it
predominantly pushes into the left
atrium bc of pressure from DV
diameter

Conversely, blood from the
inferior vena cava (IVC) flows into
the RA
Foramen Ovale

Factors contributing to closure
– Pulmonary and vascular
Resistance decreases

Physiological changes
– Increased quantity of blood into the left atrium
– Causes left atrial pressure to rise above that in
the right atrium
– Closes the flap of this one-way valve
preventing blood flow across the septum

Anatomical closure takes months or years
VIDEO BREAK
http://www.youtube.com/watch?v=wsDwQ
w1JjTU&feature=player_detailpage
http://www.youtube.com/watch?v=ZOtk_FS
fHpw&feature=player_detailpage
Persistent (Patent)
Ductus Arteriosus
Failure of closure of the vessel that joins the
pulmonary artery to the aorta
 Effects:

– Depend on size of shunt and degree of
pulmonary hypertension
 Small to moderate shunts
– Easy to fatigue, dyspnea on exertion and exercise intolerance
later in life
 Large shunts
– Poor growth and development
– Frequent episodes of pneumonitis and development of
congestive heart failure
– Life expectancy is markedly reduced – these individuals often die in
their second or third decade
Persistent (Patent)
Ductus Arteriosus

Potential causes
– Hypoxia and acidosis will increase pulmonary vascular
resistance and increase right-to-left shunting
– Higher incidence when infants are born at high
altitudes (>10,000 ft)
– Twice as common in females vs. males
– Frequency increased in preterm infants
 Fail to close spontaneously
 Closure induced with cyclooxygenase inhibiting drugs in
premature babies ONLY
– COX-1 and COX-2 are enzymes in arachidonic acid metabolism
producing producing prostaglandins, prostacyclins and
thromboxanes
– COX inhibitors are NSAIDS (ibuprofen or indomethacin)
VIDEO- watch on your own
http://www.youtube.com/watch?v=g_zQEQ
BLv_g&feature=player_detailpage
Persistent Pulmonary Hypertension
Occurs when pulmonary vascular
resistance fails to decrease
 Treatments

– Mechanical hyperventilation
– Inhaled nitric oxide
– Ventilation
– Extracorporeal membrane oxygenation
(ECMO)
– Free radical scavengers (SOD)
Persistent Pulmonary Hypertension

Mechanical
hyperventilation
– Results in alkalosis
 Improves condition as
systemic pH rises over
7.55 to 7.6
– Problems can occur if
too vigorous or sustained
too long

Inhaled nitric oxide
– Mimics endotheliumderived relaxing factor
 Promotes pulmonary
vasodilatation
 Poorly sustained
response in most
infants
Persistent Pulmonary Hypertension

Ventilation

– High oscillatory
– Effective with severe
associated lung disease
ECMO
– Infants placed on
blood bypass pump
– Blood exits the right atrium
passes through a membrane
oxygenator and returns to the
aortic arch
– Lungs are essentially at rest
– When hypertension improves –
infants are weaned off

Problems
– Used as a last resort
– Neurodevelopmental disorders
can occur
Placental Transfusion


Transfer of blood from
the placenta to the fetus
at birth
Dependent upon timing
of umbilical clamping
(1-5 minutes) after birth

Late clamping
– Increases blood volume and
RBC’s of neonate
(20-50%)
– Can increase bilirubin
concentrations

Early clamping
– Decreases blood volume
 anemia

Foals
– Early clamping leads to barker
syndrome, temporary
blindness, and dummy foal
syndrome
– Increased frequency of death
Umbilical Vessel Constriction

Factors involved
– Chemical
 Bradykinins
 Epinephrine
 Seratonin
– Mechanical
 Increase in PO2
– Humoral
 Thromboxane- blood
clotting and vessel
constriction
 Histamine- ??

If constriction does
not occur
– Persistent bleeding
leading to hemorrhage
and severe blood loss
– Potential for infection
– Surgical intervention
may be needed