L29 Maternal And Fetal Circulation Flashcards
Placenta originates from
Fetal zygote tissue during development and forms a chorionic plate of branching vessels
Becomes fully functional at end of 1st trimester
Fetal circulatory system differentiates from mesoderm of embryo
Fetal blood travels via umbilical cord which made of two umbilical arteries and a single umbilical vein
Fetal heart begins to beat in 4th week of gestation
Fetal circulation has two special circuits
Do not mix! Communicate through capillaries
Utero-placental circulation ( not fully established until end of 1st trimester)
Placental-umbilical circulation
Development of fetal zygote
Fertilized ovum divides mitotically, within a week grows and differentiates into a blastocyst capable of implantation
Blastocyst implants in endometrial lining by means of enzymes that digest endometrial tissue
Only after implantation is completed, human chorionic gonadotrophin (hCG) is detectable in maternal serum
Placental hCG signals the ovary to continue production of estrogen and progesterone
Most pregnancy tests detect placental hCG
Development of placenta
Shortly after blastocyst has implanted (6-7 days after fertilization), the syncytiotrophoblast invades the storms of uterus (decidua) forming fluid-filled holds called lacunae
Fetal circulatory system differentiates from mesoderm of embryo. Cytotrophoblasts proliferate and form chorionic villi and fetal blood vessels form within them
Lacunae become in contact with lateral blood vessels and eventually merge with one another to create intervillous space
Anatomy of placenta
Fetal side and maternal side
Fetal side develops from same blastocyst that forms the fetus and contains chorionic plate of branching vessels from umbilical cord
Lateral side develops from maternal uterine tissues and it can release substances into maternal or fetal circulations
Umbilical cord
Is lifeline that attaches fetal side of placenta to the fetus forming a chorionic plate of branching vessels
Unlike systemic arteries after birth, umbilical arteries carry deoxygenated blood. As they approach placenta they branch repeatedly forming chorionic villi that form a capillary network
Blood that has obtained sig higher O2/nutrient return to fetus from placenta through a single umbilical vein
Utero-placental circulation
Oxygenated maternal blood enters intervillous space via spiral arteries
Blood flow spreads over fetal chorionic villa toward chorionic plate then reversed direction, aided by arterial BP, intra-uterine P, and contractions of myometrium
Blood leaves through venous orifices via maternal vein
Placental-umbilical circulation
Forest of fetal chorionic villi from capillary network
Fetal blood entered through paired umbilical arteries in deoxygenated state
Oxygenated blood leaves through a single umbilical vein
Functions of placenta
Temporary organ of pregnancy with special functions
Two special circulations that don’t mix
Acts as lung to allow gas exchange
Acts as kidney to remove waste from fetal blood
Acts as GI tract to absorb nutrients from mother
Act as a barrier to protect fetus from mothers immune system
Acts as endocrine organ- source of steroids and growth factors
Cardiovascular changes during pregnancy that facilitates fetal perfusion
Maternal blood volume increases
Peripheral a vascular resistance decreases
Cardiovascular changes during pregnancy that decreases heart work
Blood viscosity decreases
Mean arterial Pressure (MAP) decreases
Changes in blood volume and viscosity
Total blood volume : 40% increase
Protects against impaired venous return when going from supine to erect position
Ameliorates parturition-associated blood loss
Blood plasma: 40-50% increase
RBC: ~30% increase
% hematocrit: decreases 2-3% (physiological anemia to minimize work of heart)
Changes in heart function during pregnancy
CO increases 30-50%
SV increases ~30% (from increase V)
HR increases ~20%
EF increases 3-5%
Ventricular volumes increases promoting frank-starling mechanisms for increased cardiac performance
Highly targeted effects in body
Renal flow increases 40% CO
Uterine flow increases 15% CO
Perfusion of heart, skin, and breasts increase
Perfusion of brain, gut, and skeleton not changed
Changes in BP and R during pregnancy
Systemic vascular resistance decreases up to 50%
Addition of parallel low R pal central circuit
Increased blood levels of estrogen and other factors (PGEs)
MAP decreases until mid pregnancy, then returns to original level
Decrease due to drop in total vascular R
Effect of adding a placenta on systemic vascular R
Adding another parallel vascular bed reduces resistance
Chemical signaling from placenta
Placental and maternal steroids increase: estrogens and progesterone
Prostaglandins gradually increase
Increased angiotensin II and aldosterone (placental RAS pathway)
Decreased sensitivity to angiotensin II in mom
Decreased norepinephrine
Endothelin-I in placental arteries and veins is a potent vasodilator
Eiconsanoids: thrombaxne present, potent vasoconstrictor and prostacyclin is a strong vasodilator
Increased NO production via eNOS expression in placental vessel endothelium
Cardiac remodeling
Increases: left ventricular wall thickness
Left ventricular mass
Valve orifice areas
Spiral artery remodeling creates a
High flow, low resistance vascular bed with steep drops in resistance from uterine arteries to the intervillous space
Uterine artery: 80-100mmHg
Spiral artery: 70mmHg
Intervillous space: 10mmHg
Preeclampsia
Elevated maternal BP
Develops in two stages:
1. Altered perfusion in circulation causes placental ischemia: placental or vascular abnormalities , deficiencies in spiral artery remodeling failing to produced conditions of high flow, low resistance (more narrow cone shaped) or placental abruption(detachment)
- Ischemic placenta releases factors that cause maternal endothelial dysfunction, vasoconstriction and hypertension (AT-1, thromboxane)
Fetal circulation: four unique shunt
Fetal heart pumps large quantities blood through placenta and smaller amount of blood through other organs
Fetal pulmonary circuit is low flow, high resistance
Enhances delivery of O2 to fetal brain
Works in parallel not series
Shunts bypass postnatal route: Placenta Ductus venosus Foramen ovale Ductus arteriosus
Placental shunt
Low resistance, high volume
Receives 50% of CCO from fetus
Shunts blood away from lower trunk and abdominal visceral (kidneys)
Umbilical veins carriers higher O2 saturated blood to fetus
Umbilical arteries carrier O2 mixed blood to placenta
Ductus venosus
Shunts blood from umbilical vein to IVC, bypassing fetal liver
Transports blood to IVC, blood from portal vein 19% CCO combined with umbilical blood (50% CCO)
IVC carries 69% CCO
Foramen ovale
Oval hole in septum diving the atria
Represents right to left shunt of well-oxygenated blood from IVC
No blood from SVC or coronaries enter foramen ovale
Of IVC blood, 27% shunts to left atrium and combined w 7% poorly-oxygenated blood from lungs
This blood enters left ventricle, 24% enters brain, upper body, coronary sinus and ~10% stays in descending aorta
Ductus arteriosus
Shunts blood 58% CO from left pulmonary artery to aorta
Represents right to left shunt
42% of IVC blood mixes w poorly oxygenated blood from SVC and enters right ventricle
Of IVC blood, 69% CCO, 27% shunts to left atrium and remaining 42% combines w 24% poorly oxygenated blood from SVC
This blood entered the right ventricle (66% CCO) where 59% is shunted to aorta and ~7% to fetal lungs
Fetal heart has higher P
On right side than left side
That’s why blood is pushed from right to left , pressure differential
Fetal heart works in parallel
Outputs of right and left hearts both deliver O2 containing blood to body
Adjustments to circulation at birth
Newborns paced with hypoxia, hypoglycemia, and hypothermia
Placenta lost, doubling total peripheral resistance
Umbilical vasoconstriction
Closure of placental circulation
Increased SA of lungs and increased return from lungs
Aortic and left atrial pressure increases
Closure of foramen ovale (reversed pressure gradient), ductus venosus (sphincter constricts~3hrs after birth) and ductus arteriosus (increased systemic resistance reverses flow via ductus arteriosus )
First breath: expansion of lungs
Pulmonary circulation opens, decreasing pulmonary vascular resistance
Pulmonary blood flow increase
Pulmonary arterial pressure (right side) decreases
RV pressure falls
Closure of foramen ovale
Decreased pulmonary P
Increased systemic resistance and increased pulmonary return leads to increase LV pressure
Closure of ductus arteriosus
Maintained open by prostaglandins during fetal life; lost after birth
At birth blood flow reverses
W/in a few hrs after birth closes functionally due to vasoconstriction in response to:
Loss of prostaglandins
Elevated PO2
Shifts from pumping in parallel to series
CO is now same btw right and left heart
Closure of ductus venosus after birth
~3hrs-18days after birth by vasoconstriction of sphincter
Closure forces blood into portal vein and into liver
Remnant of ductus venosus and umbilical vein forms ligament that divides left part of liver into medial and lateral sections = ligamentum teres hepatis
Atrial septal defect
Forman ovale didn’t close
Left to right shunt
Oxygenated blood to right atria
More blood to lungs
Leads to dilation of RA, pulmonary vessels and pulmonary hypertension
Ventricular septal defect
Hole in heart
Left to right ventricular shunt
Severity depends on size of defect
Sends oxygenated blood to RV and more blood to lungs
Overload pulmonary side, resulting in pulmonary hypertension
Increased pulmonary return to left atria
Leads to left heart remodeling
Patent ductus arteriosis
Ductus arteriosus remains open
Left to right shunt
Increase in pulmonary and right ventricle P
left heat becomes overloaded from increased volume bc increased pulmonary return
Systemic blood oxygenated normally
