3.3.2. Fetal-Neonatal Cardiovascular Trans. Flashcards

1
Q

What provides oxygen to the fetus in utero?

A

the placenta

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2
Q

Name the fetal shunts:

A
  1. ductus venosus
  2. foramen ovale
  3. ductus arteriosis
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3
Q

How is the ductus venosus involved in fetal circulation?

A

Oxygenated blood from the placenta is delivered by the umbilical vein. This blood goes through the ductus venosus and the hepatic veins and enters the inferior vena cava.

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4
Q

How is the foramen ovale involved in fetal circulation?

A

The inferior vena cava directs blood right to the foramen ovale. This allows the left side of the heart to get higher oxygenated blood than the right side (left side goes to brain which needs the oxygen). The right side gets moderately oxygenated blood which flows out the pulmonary artery towards the lungs (but will get shunted at the ductus arteriosus).

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5
Q

How is the ductus arteriosus involved in fetal circulation?

A

It allows blood to bypass the lungs and go out to the body.

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6
Q

True or false: fetal hemoglobin binds to oxygen more strongly than adult hemoglobin.

A

True

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7
Q

True or false: in adults, equal amounts of blood are pumped by both sides of the heart.

A

True

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8
Q

True or false: in fetuses, equal amounts of blood are pumped by both sides of the heart.

A

False: LV 44% work and 65% O2 saturation (low)

RV 55% work and 55% O2 saturation (low)

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9
Q

What are the relative resistance changes to the circulation system that happen at birth?

A
  • When the umbilical cord is clamped, the systemic circulation immediately becomes high resistance
  • Lungs inflate and pulmonary arterioles relax, resulting in lower resistance.
  • in a nutshell: the relative resistances of the pulmonary and systemic circuits reverse*
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10
Q

Why is it so important that pulmonary vascular resistance drops after birth?

A

-The RV is an inefficient pump (not nearly as good as the LV at pumping) so when pulmonary vascular resistance is elevated, the RV is stressed and may fail to pump forward. Other complications include RV arrhythmia (both of these complications can be fatal). Essentially, the RV will “wear out” over time if asked to do the hard work that the LV does.

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11
Q

Why are abrupt changes in pulmonary vascular resistance dangerous?

A

They may cause immediate stretch of the RV, leading to a fatal arrhythmia (the neonate therefore has a biphasic change in pulmonary resistance. First there is an initial drop in PVR, then there is a gradual process that lowers it to adult levels over the course of 4-6 weeks).

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12
Q

What are the relative pressures of the 4 chambers of the heart by 4-6 weeks of age?

A
Use the mnemonic: "nickel, dime, quarter, dollar"
RA--0.05
LA--0.10
RV--0.25
LV--1.00
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13
Q

How are the shunts affected when the umbilical cord is clamped at birth?

A
  • clamping the umbilical cord stops ductus venosus flow because it was coming from the umbilical vein
  • this also lowers the right atrial pressure, helping to close the foramen ovale
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14
Q

What keeps the ductus arteriosus open in-utero, and what is it’s physiological mechanism?

A

Prostaglandin E (PGE) which is produced in the placenta (there is some fetal production as well but it is unclear where). PGE is a potent vasodilator.

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15
Q

What contributes to the 2 phases of postnatal closure of the ductus arteriosus?

A
  1. Constriction: placental source of PGE removed, increased flow to the lung breaks down more PGE (PGE is destroyed in the lungs), higher oxygen content encourages ductal constriction (takes a few days to close)
  2. Remodeling: infiltration by fibrocytes, hypertrophy of endothelium–> leads to the transformation into the ligamentum atrteriosum (takes 2-3 weeks to obliterate ductal lumen)
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16
Q

What happens when the ductus arteriosus does not close correctly after birth?

A

Persistent Pulmonary Hypertension of the Newborn (PPHN)

17
Q

What is involved in Persistent Pulmonary Hypertension of the Newborn (PPHN)?

A
  • hypoxia at birth causes pulmonary arterioles to remain constricted
  • since PVR>SVR, ductus arteriosis shunting is from pulmonary artery to the aorta
  • minimal lung blood flow leads to profound hypoxia and acidosis
18
Q

What do we use to treat PPHN?

A
  1. oxygen: helps fully saturate blood that reaches lungs AND is a pulmonary vasodilator
  2. nitric oxide: potent vasodilator
  3. vasopressors: increase systemic pressure and you push more blood towards the lungs by opposing R-L shunting through PDA
19
Q

When would it be helpful to have a ductus arteriosis stay open?

A
  1. congenital heart disease
  2. often, heart defects are ductal depependent
  3. hypoplastic left heart syndrome
20
Q

What is involved in Hypoplastic Left Heart Syndrome?

A
  • small LV, closed PDA,
  • results in no blood to the head OR vital organs
  • without treatment (or without PDA or ASD), baby will die
21
Q

What can be used to help treat Hypoplastic Left Heart Syndrome at birth?

A
  • Give PGE to prolong shunts after birth (to allow some systemic blood flow)
  • Surgical: Norwood procedure, Fontan procedure
22
Q

What does the Norwood procedure achieve (a surgical treatment of Hypoplastic Left Heart Syndrome)?

A
  • creates a neo-aorta
  • RV does the work of both sides of the circuit
  • best O2 saturation is around 80% (not well)
  • an acceptable fix until the Fontan procedure can be done (final stage of preparing kids for normal life–these patients will then have normal O2 saturations)
23
Q

What is Ductal-dependent Pulmonary bloodflow (or Hypoblastic Right Heart Syndrome)?

A
  • pulmonary atresia with intact ventricular septum
  • blood will be cut off at pulmonary valve, so need an alternate root
  • Solution: to keep PDA in order to allow blood flow to the lungs