Cardiovascular, pg 1 of 11
Congenital Heart Defects
We don’t know entirely what cause congenital heart defects
• 90% Idiopathic Etiology
• Factors associated w/ increased incidence of CHD:
• Fetal/maternal infection in 1st trimester has a big bearing on the unborn child. By 5th week heart is beating...a
lot of women don’t even know they’re pregnant yet at that point.
• Parent alcoholism (both parents contribute...alcohol makes male sperm abnormal)
• Parent use of drugs w/ teratogenic effects
• Cocaine does attack to the sperm!
• Maternal smoking or exposure to second hand smoke during pregnancy
• Maternal age over 40 yr
• Statistics can be fudged to show a lot of different things
• The reason for this one is b/c there are fewer births after this age
• More cases of DS prior to 35 b/c more births at that time
• If male is over 55 more cases of DS
• Maternal dietary deficiencies
• Maternal IDDM
Congenital Heart Defects
• 35 are recognized
• 9 are common (represents 90% of the CHDs)
Need to Understand…
• “Normal circulation”
• Fetal circulation
• Postnatal circulation...where the pressures are, where it’s going, where is the oxygenated blood...where is the
unoxygenated blood.
• Pressure differences in the heart
Fetal Circulation
Oxygenated blood from the placenta is carried to the fetus by the umbilical vein. Somewhere between 50 & 80% of
this blood enters the ductus venosus and is carried to the inferior vena cava (the rest goes through the liver). From
the IVC the blood goes to the right atrium of the heart, and most goes through the foramen ovale to the left atrium
(bypassing pulmonary circulation), which means the left atrium now has oxygen-rich blood. The blood then goes into
the left ventricle, and is then pumped into the aorta into the body.
The blood coming from the head and upper extremities enters the right atrium from the SVC and does not go through
the foramen ovale, but instead enters the right ventricle and is pumped into the pulmonary artery. There is an
opening between the pulmonary artery and the aorta called the ductus arteriosus, which directs most of this blood
away from the lungs to bypass pulmonary circulation.
Pressures in the heart
• Before birth there is high pulmonary resistance b/c the fetal lung is collapsed.
• This high pulmonary pressure causes greater pressures in the right side of the heart and pulmonary arteries.
• The free-flowing placental circulation and the ductus arteriosus produce a low vascular resistance in the remainder
of the fetal vascular system.
• When the umbilical cord is clamped and the lungs expand at birth, the hemodynamics of this sytem undergo some
rapid and pronounced changes. The pulmonary pressure goes down, and systemic pressure goes up. This causes
the higher pressure to now be on the left side of the heart (this makes sense because the left ventricle has to push
very hard to get blood out to the whole system...it needs a lot of pressure to make that happen). When this
pressure change happens, it closes the foramen ovale by shutting the little leaflet flaps shut. Note that this may not
happen instantly and may take a few hours or even a few days.
• Recall that blood is going to flow from an area of high pressure to an area of low pressure...think of your garden
hose. It has high pressure and it pushes the water out!
, Cardiovascular, pg 2 of 11
• Normally, the pressure on the right side of the heart is lower than the left; and resistance in the pulmonary system
is less than in systemic circulation.
Differences between fetal circulation and normal neonatal circulation
• Ductus venosis: This is a blood shunt between the left umbilical vein and the inferior vena cava which empties into
the right atrium. This blood coming in is baby’s blood...it has come from the placenta and has nutrients. This
eventually becomes the belly button!
• Foramen ovale: is between the two atria. In utero it shoots straight across...the gradient of pressure is right to left.
It bypasses the lungs. There is high resistance in pulmonary area, so blood doesn’t go to lungs.
• Patent ductus arteriosis is between the aorta and the pulmonary artery. The blood is going from the pulmonary
artery across to the aorta b/c this is oxygen rich blood and going out to systemic circulation. There is low systemic
resistance in fetus. The patent ductus arteriosis is sensitive to oxygen...so as soon as the baby takes his first
breath, this opening closes (or should close).
Review: Postnatal
• Breath: Hypo- to hyper-oxygenation
• PO2: Goes from the 40s to 70s or 80s immediately
• Ductus arteriosus – begins to constricts (can take up to 72 hours), may take longer to close in a premie. A baby
with a PDA will have a murmur.
• Pulmonary vascular bed opens
• Pulmonary vascular resistance decreases (recall that it was high before!)
• Systemic vascular resistance increases (remember it was low before)
• Foramen ovale closes d/t blood flow left to right.
Assessment
• History
• Physical exam
• Murmurs and cyanosis don’t always happen immediately. A large murmur is going to be “soft”.
• Determine if the issue is cardiac vs respiratory
• Often can look the same; the systems are interdependent
• How do you figure out the difference? Compare and contrast the…
• Color: Are they blue and where are they blue? Cyanosis is a common feature of CHD, and pallor is a sign
of poor perfusion.
• Are they cold?
• Are they acidotic?
• What was the labor like? If it was long...they can become acidotic b/c the lack of oxygen causes
hypoxia...if they come out acidotic, it’s going to take them a while to pink up.
• Is there a murmur?
• Listen to lungs: If child was born via C/S you will hear fluid b/c not getting squeezed out when going
through vaginal canal. We call these “gunky babies” bc they have a lot of fluid...this child will need more
suctioning.
• Pulses...on a newborn you’re going to check pulses at bracheal and femoral...want to see if pulses are
same upper vs. lower...if not, then a cardiac defect is present. Be aware that chubby babies are hard to
get pulses on (no duh!)
• BP: take BP on all four extremities b/c you can pick up one of the defects this way.
• What if baby cries: If a respiratory issue, the child should turn pink when crying b/c he is taking a big
breath; a cardiac baby will turn bluer b/c the increased breath isn’t making a difference. The problem is
that they are having trouble moving the oxygenated blood around.
• Give baby 100% oxygen even though they don’t have a respiratory issue. This decreases the cardiac
workload. If you put the oxygen on a respiratory kid, the O2 sats will go up pretty quickly, but will stay the
same if you put it on a cardiac kid. If you don’t give adequate oxygen, the pulmonary beds constrict and
this is most likely not a very good thing.
• Blood Gases: on respiratory baby the O2 will be low, CO2 will be high; in cardiac kid the O2 will be low b/c
blood not coming around like it should, and CO2 will be normal b/c they are able to blow it off.
Congenital Heart Defects
We don’t know entirely what cause congenital heart defects
• 90% Idiopathic Etiology
• Factors associated w/ increased incidence of CHD:
• Fetal/maternal infection in 1st trimester has a big bearing on the unborn child. By 5th week heart is beating...a
lot of women don’t even know they’re pregnant yet at that point.
• Parent alcoholism (both parents contribute...alcohol makes male sperm abnormal)
• Parent use of drugs w/ teratogenic effects
• Cocaine does attack to the sperm!
• Maternal smoking or exposure to second hand smoke during pregnancy
• Maternal age over 40 yr
• Statistics can be fudged to show a lot of different things
• The reason for this one is b/c there are fewer births after this age
• More cases of DS prior to 35 b/c more births at that time
• If male is over 55 more cases of DS
• Maternal dietary deficiencies
• Maternal IDDM
Congenital Heart Defects
• 35 are recognized
• 9 are common (represents 90% of the CHDs)
Need to Understand…
• “Normal circulation”
• Fetal circulation
• Postnatal circulation...where the pressures are, where it’s going, where is the oxygenated blood...where is the
unoxygenated blood.
• Pressure differences in the heart
Fetal Circulation
Oxygenated blood from the placenta is carried to the fetus by the umbilical vein. Somewhere between 50 & 80% of
this blood enters the ductus venosus and is carried to the inferior vena cava (the rest goes through the liver). From
the IVC the blood goes to the right atrium of the heart, and most goes through the foramen ovale to the left atrium
(bypassing pulmonary circulation), which means the left atrium now has oxygen-rich blood. The blood then goes into
the left ventricle, and is then pumped into the aorta into the body.
The blood coming from the head and upper extremities enters the right atrium from the SVC and does not go through
the foramen ovale, but instead enters the right ventricle and is pumped into the pulmonary artery. There is an
opening between the pulmonary artery and the aorta called the ductus arteriosus, which directs most of this blood
away from the lungs to bypass pulmonary circulation.
Pressures in the heart
• Before birth there is high pulmonary resistance b/c the fetal lung is collapsed.
• This high pulmonary pressure causes greater pressures in the right side of the heart and pulmonary arteries.
• The free-flowing placental circulation and the ductus arteriosus produce a low vascular resistance in the remainder
of the fetal vascular system.
• When the umbilical cord is clamped and the lungs expand at birth, the hemodynamics of this sytem undergo some
rapid and pronounced changes. The pulmonary pressure goes down, and systemic pressure goes up. This causes
the higher pressure to now be on the left side of the heart (this makes sense because the left ventricle has to push
very hard to get blood out to the whole system...it needs a lot of pressure to make that happen). When this
pressure change happens, it closes the foramen ovale by shutting the little leaflet flaps shut. Note that this may not
happen instantly and may take a few hours or even a few days.
• Recall that blood is going to flow from an area of high pressure to an area of low pressure...think of your garden
hose. It has high pressure and it pushes the water out!
, Cardiovascular, pg 2 of 11
• Normally, the pressure on the right side of the heart is lower than the left; and resistance in the pulmonary system
is less than in systemic circulation.
Differences between fetal circulation and normal neonatal circulation
• Ductus venosis: This is a blood shunt between the left umbilical vein and the inferior vena cava which empties into
the right atrium. This blood coming in is baby’s blood...it has come from the placenta and has nutrients. This
eventually becomes the belly button!
• Foramen ovale: is between the two atria. In utero it shoots straight across...the gradient of pressure is right to left.
It bypasses the lungs. There is high resistance in pulmonary area, so blood doesn’t go to lungs.
• Patent ductus arteriosis is between the aorta and the pulmonary artery. The blood is going from the pulmonary
artery across to the aorta b/c this is oxygen rich blood and going out to systemic circulation. There is low systemic
resistance in fetus. The patent ductus arteriosis is sensitive to oxygen...so as soon as the baby takes his first
breath, this opening closes (or should close).
Review: Postnatal
• Breath: Hypo- to hyper-oxygenation
• PO2: Goes from the 40s to 70s or 80s immediately
• Ductus arteriosus – begins to constricts (can take up to 72 hours), may take longer to close in a premie. A baby
with a PDA will have a murmur.
• Pulmonary vascular bed opens
• Pulmonary vascular resistance decreases (recall that it was high before!)
• Systemic vascular resistance increases (remember it was low before)
• Foramen ovale closes d/t blood flow left to right.
Assessment
• History
• Physical exam
• Murmurs and cyanosis don’t always happen immediately. A large murmur is going to be “soft”.
• Determine if the issue is cardiac vs respiratory
• Often can look the same; the systems are interdependent
• How do you figure out the difference? Compare and contrast the…
• Color: Are they blue and where are they blue? Cyanosis is a common feature of CHD, and pallor is a sign
of poor perfusion.
• Are they cold?
• Are they acidotic?
• What was the labor like? If it was long...they can become acidotic b/c the lack of oxygen causes
hypoxia...if they come out acidotic, it’s going to take them a while to pink up.
• Is there a murmur?
• Listen to lungs: If child was born via C/S you will hear fluid b/c not getting squeezed out when going
through vaginal canal. We call these “gunky babies” bc they have a lot of fluid...this child will need more
suctioning.
• Pulses...on a newborn you’re going to check pulses at bracheal and femoral...want to see if pulses are
same upper vs. lower...if not, then a cardiac defect is present. Be aware that chubby babies are hard to
get pulses on (no duh!)
• BP: take BP on all four extremities b/c you can pick up one of the defects this way.
• What if baby cries: If a respiratory issue, the child should turn pink when crying b/c he is taking a big
breath; a cardiac baby will turn bluer b/c the increased breath isn’t making a difference. The problem is
that they are having trouble moving the oxygenated blood around.
• Give baby 100% oxygen even though they don’t have a respiratory issue. This decreases the cardiac
workload. If you put the oxygen on a respiratory kid, the O2 sats will go up pretty quickly, but will stay the
same if you put it on a cardiac kid. If you don’t give adequate oxygen, the pulmonary beds constrict and
this is most likely not a very good thing.
• Blood Gases: on respiratory baby the O2 will be low, CO2 will be high; in cardiac kid the O2 will be low b/c
blood not coming around like it should, and CO2 will be normal b/c they are able to blow it off.
