Cp2.5, Dr Ballam, Fetal To Adult Basics, Post Midterm

Front 1

Which ventricle in fetus has to generate high pressures?

Back 1

In the fetus the right side of the heart has more pressure

Front 2

Ductus arteriosis

Back 2

fetal vascular channel connects the pulmonary artery to the aorta. since the pressure is greater in pulmonary artery if flows from pulmonary artery to the aorta

Front 3

When you add a placenta to circulation, resistance goes...

Back 3

down. Systemic circulation is lower resistance in fetus than in adult.

Front 4

foramen ovale

Back 4

shunts blood between right atrium and left atrium

Front 5

in birth when umbilical arteries and veins are clamped this causes

Back 5

increase in fetal total peripheral resistance. followed by closure of ductus venosus. lungs expand and pulmonary resistance falls.. Now the Left ventricle generates much greater pressure than the right.

Front 6

tetralolgy of fallot. what causes it? what is the outcome?

Back 6

comes from inappropriate junctioning of the septum.
1) ventricular septal defect
2) RV hypertrophy
3) constriction of right ventricle ejection tract
4) aorta positioned over incomplete septal wall

Front 7

flow across a vascular bed is dependent upon

Back 7

1) arterial pressure-venous pressure
2) resistance through the tissue
3) # and diameter of vessels
Flow= (change pressure)/resistance

Front 8

cardiac output

Back 8

blood pressure/total peripheral resistance. BP=arterial pressure and assume that venous pressure is zero

Front 9

adult systemic pressure in large arteries, arterioles, capillaries and vena cava

Back 9

120/80 in large arteries
66/60 in arterioles
18 in capillaries
0-4 in vena cava

Front 10

pulmonary circulation pressures in adult large arteries, capillaries and veins

Back 10

24/16 in large arteries
capillaries=8
veins = 6 (left filling pressure)

Front 11

Adult average resistance is

Back 11

1 with a range of 0.2 (low) to 4 (high)

Front 12

short term and long term control of BP are controlled by..

Back 12

short term=sympathetic NS
long term=renin-angiotensin system

Front 13

the umbilical artery carries...

Back 13

deoxygenated blood from the fetus to the placenta

Front 14

the umbilical vein carries.

Back 14

oxygenated blood from the placent back to the fetus

Front 15

the umbilical vein connect to..

Back 15

the fetal inferior vena cava in the liver

Front 16

the foramen ovale

Back 16

allows blood to pass from the right atrium directly to the left atrium thus bypassing the right heart and lungs

Front 17

In the fetus which has greater pressure the right or left atrium Why?

Back 17

The right is higher because the lungs are collapsed which causes a large resistance against which the right ventricle must work to get blood through. presures in fetal right atrium and ventricle are greater than in the adult

Front 18

ductus arteriosis (what is it and what keeps it open)

Back 18

connects the pulmonary artery to the aorta. maintained open by prostaglandins and low PO2

Front 19

when the umbilical arteries and veins are clamped this causes ____ in fetal TPR

Back 19

an increase

Front 20

When fetal lungs expand what happens to pulmonary resistance?

Back 20

It falls

Front 21

Since TPR increases in the baby post-parturition what happens to blood flow?

Back 21

Left ventricle works harder to pump against the increased TPR. The right ventricle doesn't have to work as hard now that the lungs have expanded. The foramen ovale now closes because of this change in pressure gradient. Since left pressure > right pressure flow reverses through the ductus arteriosis and passes from the aorta into the pulmonary artery.

Front 22

When flow changes through the ductus arteriosis what kind of a shunt is this?

Back 22

left to right shunt. (blood now going from L side of heart to the R side, aorta-->pulmonary)Within a few days hormone changes and increased arterial O2 sat passing through the ductus arteriosis causes it to close.

Front 23

What 2 major factors cause a change in blood flow pattern following birth?

Back 23

systemic vascular resistance is increased due to removal of placental circulation.
decreased resistance of the pulonary circulation due to expansion and oxygenation

Front 24

cyanotic vs acyanotic

Back 24

acyanotic=no left to right shunt
cyanotic=usually a right to left shunt

Front 25

acyanotic

Back 25

blood passes from systemic circulation to pulmonary circulation withought passing through systemic perfusion bed for gas exchange (not blue because the blood still has O2 in it)

Front 26

cyanotic

Back 26

blood passes from right heart to systemic circulation without passing through gas exchange surfaces of lungs. turn blue because no O2 onloaded to bloos

Front 27

What kinds of defects can lead to an acyanotic problem

Back 27

atrial septal defect=L to R shunt
ventricular septal defect
patent ductus arteriosis
aortic stenosis
post ductal coarctation of the aorta, pulmonic stenosis

Front 28

atrial septal defect

Back 28

is a left to right shunt. oxygenated blood passes fro left to right atrium to be reoxygenated. elevated pressures and dilation of right atrium and ventricle occur

Front 29

ventricular septal defect

Back 29

blood passes from LV to RV in a left to right shunt. all chambers may dilate due to increased pressure of RV and increased return to LV. LV dilation can lead to heart failure. Prolonged severe shunt may cause increased pulmonary resistance and reversal of shunt.

Front 30

patent ductus arteriosis

Back 30

blood passes from aorta into pulmonary artery. L to R shunt. May cause LV dilation due to increased return. May lead to heart failure.

Front 31

aortic valve stenosis

Back 31

usually failure of proper aortic valve development--bicuspid valve. no shunt if minor but if severe causes R to L shunt through ductus arteriosis and possible L to R shunt via foramen ovale. High LV systolic pressures, low post stenosis pressure and LV hypertrophy

Front 32

coarctation of the aorta

Back 32

similar effect on LV as aortic stenosis. usually occurs after branching to head and upper extremities. if postductal=no shunt. if preductal=ductus may remain open. if severe enough it can cause R to L shunt and cyanosis

Front 33

pulmonic valve stenosis

Back 33

high RV pressure b/c resistance to flow past pulmonic valve. low pulmonary artery pressures, RV hypertrophy. if back up into RA then may have R to L shunt through atrial septal defect due to elevated atrial pressures

Front 34

What defects can happen and cause a cyanotic lesion?

Back 34

tetralog of fallot
ASD (R to L shunt)
preductus coarctation of aorta
transposition of great vessels

Front 35

tetralogy of fallot

Back 35

1) VSD
2) constricted RV tract=increased resistance to RV ejection, increased RV pressure, R-->L shunt, decreased pulmonary artery pressure
3) aorta positioned over incomplete septal wall
4) RV hypertrophy

Front 36

transposition of great vessels

Back 36

parallel circuits, blood passes from pulmonary veins to LV-->lungs-->LV
blood passes from vena vavae to RV to systemic circulation to RV
not serious in fetus because blood mixes in ductus arteriosis and foramen ovale and they have the placenta. After birth can only live short period which is extended if patent ductus or foramen ovale allows mixing of blood.