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| - | *continued here from [[Lecture 10 Coronary Artery Disease]] on 01/31/11 at 9:45AM.
| + | 1t98xD I truly appreciate this blog. |
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| - | ==Fetal and Neonatal Cardiovascular Physiology==
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| - | *We'll talk about the fetus but really mom even more.
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| - | ===Objectives===
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| - | *In the fetus, why does the head, heart, and upper torso receive blood with a higher oxygen content than in the lower body?
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| - | *What two anatomical structures are open to blood flow in the fetal circulation but close after birth? What is the function of each of these structures? By what mechanism does each of these open structures close after birth has occurred?
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| - | *How does the right ventricle contribute to perfusion of the fetal body? How does blood from the right ventricle reach the aorta?
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| - | *What unusual property of fetal hemoglobin compared to adult hemoglobin makes oxygenation of the fetus possible?
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| - | *At what point during the birth process does the neonate stop receiving oxygen from the mother? What is the stimulus for the fetal placental circulation to shut down?
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| - | *How does the mother's cardiac output, vascular resistance, and mean arterial blood pressure change during the course of pregnancy? What are the three major reasons that the cardiac output increases? How much does pregnancy increase oxygen usage by the mother?
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| - | *How does the fetus receive glucose, amino acids, and monoglycerides from the mother's blood? Which of these materials is the major source of nutrition?
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| - | *Why cardiac output decrease in the supine position as pregnancy advances and the fetus/uterus enlarges? How do women compensate for this problem?
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| - | *How much does the mother's blood volume increase on average during pregnancy? How much does total extracellular volume increase in support of the fetus?
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| - | ===I. Fetal blood flow pathways===
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| - | ====A. The fetal placenta receives approximately 45% of the fetal cardiac output====
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| - | *As the fetus sits around in the womb.
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| - | *The cardiovascular system is little odd:
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| - | **Ductus areteriosa sends blood from pulmonary artery to the aorta because we don't want to perfuse the lungs.
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| - | ***Only about 7% of total cardiac output goes into lungs
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| - | **Placenta hooks up both mom and baby circulation so baby's blood can get oxygen and such.
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| - | **The atrial septum has a hole that allows much of the blood to move from the right atrium to the left atrium.
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| - | ***Fetus puts about 60-70% of blood in pulmonary artery dispite the septal hole, so ductus arteriosus is very important.
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| - | ***This is a second mechanism by which we keep from perfusing the lungs.
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| - | **once the blood is pumped, about 45 % is send to placenta, the other 55% goes to the fetus.
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| - | ***This is important for exchanging CO2 for oxygen.
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| - | **As a result of all the shunts, the RV is dominant, not the LV as in life post-partum.
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| - | ***Therefore, babies have RV hypertrophy.
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| - | ***So their EKG has a right axis deviation.
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| - | ***This goes away after 2-3 months.
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| - | ***Left ventricle pumps about 34% of total cardiac output
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| - | ====B. Oxygenated venous blood from the placenta does not completely mix with vena cava blood====
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| - | *There isn't a large change in oxygen concentration over the placenta.
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| - | **So we have to have lots of flow through the placenta to get enough oxygen for the fetus.
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| - | **Generates oxygen saturation of about 70%
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| - | *Oxygenated blood goes to RA, gets mixed with used blood.
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| - | *Once in the PA, the saturation is about 55%.
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| - | **This would be a problem because it's too low for the brain to develop.
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| - | **But the brain ''does get enough blood'' because more of the 70% blood from the IVC than of the 40% blood from the SVC goes to the left atria (and on to the LV, aorta, and brain).
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| - | ***That is, the blood isn't fully homogenized (in terms of saturation) until after having passed the septal passage between the atria.
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| - | ***This generates 65% saturation for the brain.
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| - | *Then after the DA, the saturation is at 60%.
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| - | **This will be used by the lower body.
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| - | *Fetal blood is different than maternal blood so that it can take oxygen from the mother's blood.
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| - | **This is a matter of using a different Hb isomer with a higher affinity for oxygen.
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| - | **There is also better unloading of oxygen at the fetal tissue (periphery).
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| - | *Fetal Hb would make Everest easier.
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| - | *Have to get rid of it after we're born.
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| - | **BAby turns yellow after born because fetal Hb is being broken down.
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| - | **Can happen so fast that the baby can get sick.
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| - | **Put under blue lights to help activate vitamin D to help with Hb breakdown.
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| - | *stopped here on 01/31/11 at 10AM.
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| - | *started here on 01/31/11 at 11AM.
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| - | *Don't assume you don't have to be at CPS.
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| - | *Check IUPUI website for class closure.
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| - | ===II. Exchange across the placenta===
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| - | *Getting nutrition over the placenta is not to difficult, really.
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| - | *The placenta, on the baby's side, looks like trees with intestinal villi on the end of them.
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| - | **The mother's blood circulates around these trees.
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| - | **The baby's arterial and venous vessels that go out into the trees and the mother's blood flows all around.
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| - | **This is where exchange occurs.
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| - | *Glucose transport:
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| - | **Babies need lots of glucose for them to grow quickly.
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| - | **Glucose is the major energy molecule for the fetus, so there is lots of glucose moving from mother to baby.
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| - | **Non-insulin dependent GLUT transporters move glucose across the blood streams
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| - | ***Not Glut4 but Glut2 and others.
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| - | **For healthy baby and mom, this si good.
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| - | **If mom has diabetes (gestational or not), the baby gets quite large.
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| - | *Amino acid transport:
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| - | **There is active transport of aas from mom to baby.
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| - | **Hence, the baby's blood has higher concentrations of most aas.
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| - | *Lipid transport:
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| - | **FFAs and glycerol freely diffuse from mother to baby.
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| - | **There is some phenomenon that slows the diffusion of TAGs from mom to baby.
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| - | ===III. Maternal Cardiovascular Consequences of Pregnancy===
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| - | *Pregnancy increases demands on mom's CV system.
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| - | *Supine position causes uterus to put pressure on the vena cava.
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| - | **Some women get a sensation of lower-body numbness because blood return from lower body is impinged by baby.
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| - | **Women learn quickly lie on their sides.
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| - | **This happens in obese people, too.
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| - | *Cardiac output increases:
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| - | **The increase in output is comparable to the increase in output needed to maintain a slow walk.
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| - | ***Heart will enlarge becuase she is basically doing exercise all the time.
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| - | **Stroke volume increases, then levels off or lowers toward normal
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| - | ***Once back to normal or leveled off, the increasing heart rate maintains an increase in cardiac output throughout gestation.
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| - | **Mother's heart rate increases as baby grows.
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| - | ***This increase in heart rate should be small, though.
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| - | **Blood volume increases
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| - | ***Increases by about 1 liter (about a 25% increase for most women)
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| - | **Extracellular water content increases
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| - | ***Goes up to 6-7 liters, an increase of about 4 liters.
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| - | ***This volume is distributed between the mom, the baby, and the amniotic fluid.
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| - | **RBC mass increases
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| - | ***Plasma volume is changing along with increased RBC mass, so hematocrit actually ends up decreasing.
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| - | ***We always tell moms to take iron supplements because of all the extra RBC production.
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| - | ====G. Ideally, the mean arterial blood pressure should be relatively constant====
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| - | *In a healthy pregnancy, the mean alterial pressure should remain about the same as before pregnancy.
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| - | *Typically it goes up a few mmHg.
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| - | *If it goes up too much, it could stress mom and the baby.
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| - | **Mom has lots of extra fluid and is working really hard to push it around.
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| - | *Most women get some edema in the lower body.
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| - | ====H. Increased cardiac output offset by lowered system vascular resistance====
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| - | *While the mother's CV system is compensating in many ways to increase cardiac output (see above), the '''systemic vascular resistance''' (SVR) is also decreasing.
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| - | *This makes sense as a compensation mechanism for the increased resistance of adding a new, growing organ and a parasite (uterus and fetus).
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| - | **At term, a healthy uterus and <strike>parasite</strike> baby will receive 17-20% of the mother's cardiac output.
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| - | *Furthermore, decreased systemic vascular resistance is needed as vasodilation at the skin will be increased in order to release heat generated by pregnancy.
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| - | *There is often weight gain, either fat or muscle.
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| - | *Vascular resistance has dropped like a rock by 20 weeks.
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| - | ====I. Gradual increase in SVR after 20 weeks is not well understood====
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| - | *At 20 weeks there is a gradual increase in the systemic vascular resistance.
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| - | *It is not currently understood why resistance would increase.
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| - | *It may be a stress response to holding a huge fetus.
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| - | *If it goes up too much it can cause hypertension so we watch to be sure it doesn't get out of control because that's bad for mom and the baby.
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| - | ====J. Mother's oxygen consumption increases====
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| - | *The mother will increase her oxygen consumption about 50% of the course of gestation.
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| - | *The increased oxygen supports:
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| - | **the developing fetus,
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| - | **mom's increased CV oxygen demand,
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| - | **mom's increased body mass oxygen demand,
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| - | **mom's increased renal oxygen demand.
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| - | ===IV. Circulatory changes at birth===
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| - | *Suddenly the fetus is a baby and it must switch from the the placental vasculature (bypassing the pulmonary circuit) to the pulmonary vasculature.
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| - | *Most babies breath on their own, but may be stimulated (slap on the butt).
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| - | *There are several phenomenons that make this switch possible.
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| - | *First, when the lung expands with air, the vascular resistance in the pulmonary system drops dramatically, making it an easy, tempting route for blood flow.
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| - | *Second, the ductus arterious closes such that blood is no longer shunted away from the pulmonary arteries into the aorta.
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| - | **This occurs as PGE2 (prostaglandin E2, a vasodilator) levels decrease because the lung tissue is becoming less hypoxic.
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| - | **Increased levels of bradykinin (a vasodilator '''except in the ductus arteriosus''') may also help the ductus arteriosus close.
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| - | **As bradykinin goes up after birth, it may be part of the reason the ductus arteriosus closes.
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| - | **These are made by endothelial cells while they are in the womb, a low oxygen environment (for the pulmonary arteries).
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| - | *Third, as plasma oxygen levels rise in the baby, vessels leading to the placenta constrict and arrest blood flow to the placenta / mother.
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| - | **This occurs as a result of increased oxygen in the blood going to the placenta; '''oxygen is a very potent vasoconstrictor'''.
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| - | **Through the process of giving birth, the placental vessels continue to flow, however, keeping the baby perfused with oxygen.
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| - | *Fourth, the flap at the foramen ovale mechanically closes (and later seals).
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| - | **This occurs because pulmonary arterial resistance drops, more blood flows through the right ventricle, and the pressure in the right atrium becomes lower than the left atrium.
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| - | **This is also encouraged as blood goes through the pulmonary system and comes flying into the left atrium and slaps the flap shut.
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| - | **Also, as PGE2 (a vasodilator) decreases, the foramen ovale constricts
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| - | **5% of humans' foramen ovale do not seal.
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| - | **Once in a while the ovale opens and must be fixed surgically.
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| - | *Fifth, the baby will gradually produce adult Hb (alpha-beta as opposed to alpha-gamma).
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| - | *Sixth, the pulmonary arterioles will lose their heavy muscle layer (which has helped keep them constricted throughout development).
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| - | **During fetal life, these arteries are quite constricted.
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| - | **Pulmonary arterioles don't like oxygen; they do strange stuff in the presence of oxygen.
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| - | **So suddenly, in this baby, the blood to the pulmonary arterioles goes from being slightly oxygenated to hardly oxygenated at all; thus the arterioles dilate.
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| - | **This will help reduce pulmonary resistance making it easier for the right ventricle to push blood through.
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| - | **The right ventricle will atrophy back to a normal size over the first months as the left ventricle hypertrophies to become the dominant ventricle.
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| - | ===Clinical case===
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| - | *pulsing murmur
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| - | *full term
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| - | *sounds like a bee
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| - | *not cyanotic or hypoxic
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| - | *heart rate is high
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| - | *arterial pressure is below normal
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| - | *sympathetics are up
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| - | *What's the problem?
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| - | *A. aortic valve incompetence requiring valve replacement/repair.
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| - | ** wouldn't make a constant noise but an intermittent noise
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| - | *B. open atrial septum defect requiring catheter placement of patch.
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| - | ** could you hear this? there is very little pressure so unlikely.
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| - | *C. mitral valve stenosis requiring valve replacement/repair.
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| - | ** again, would be intermittent
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| - | '''*D. open ductus arteriosus treated with cycloxygenase blocking drug.'''
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| - | **Cox2 inhibited will decrease PGE2 production and will allow the ductus arteriosus to close.
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| - | **Noise is from fast rushing of blood
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| - | **During ventricular systole, the blood runs backward from aorta into ductus and into the lungs.
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| - | **This is usually enough to make the ductus contract if the PGs will get out of the way.
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| - | **Can close with drug or with catheter or even tie it off.
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| - | *E. coarctation (partial constriction) of the ascending aorta requiring aortic resection.
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| - | ** could happen, probably wouldn't cause constant noise, only during systole
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| - | ===Clinical case===
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| - | *27 yo prego
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| - | *first child
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| - | *light headed when lying down
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| - | *arterial pressure standing is 120/70, 87bpm
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| - | *artieral pressure sitting is lower, slower
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| - | *lying down, pressure goes up and heart rate goes up
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| - | **This is opposite of what should happen.
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| - | *What's the problem?
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| - | *A. failure of baroreceptor function.
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| - | **Probably not because they work between standing and sitting.
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| - | *B. vena cava compression by the uterus/fetus.
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| - | **Obviously this is the answer.
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| - | **Uterus presses on VC and stops some venous return from lower legs.
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| - | **Even when standing, the uterus can press on the VC such that the lower body pressure goes up.
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| - | ***Common to have distended veins in legs.
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| - | ***Common to have hemerhhoids.
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| - | *C. early heart failure due to pregnancy demands.
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| - | **No, her bp is ok, her heart rate is ok.
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| - | *D. relative hypovolemia for her stage of pregnancy.
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| - | **If this were true, she would have more trouble standing than lying down.
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| - | *E. a pulmonary artery clot that blocks by body position.
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| - | **Can't totally get rid of this because this could happen.
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| - | **Ladies do clot more readily.
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| - | **It could be a clot that when standing or sitting it hangs in just such a way that it doesn't block the flow but when supine it does.
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| - | *continued on to [[Lecture 12 Heart Defects]] on 01/31/11 at 11:25AM.
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