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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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| - | ===II. Exchange across the placenta===
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| - | A. Non-insulin dependent GLUTs primarily used to move glucose across membranes - glucose is main energy source for fetus
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| - | B. Amino acid transport from mom to baby by active transporters - fetal blood has higher amino acid concentration for most amino acids than mother's blood
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| - | C. Free fatty acids and glycerol enter baby by diffusion, something slows diffusion of triglycerides
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| - | cardiac output increase during gestation
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| - | ===III. Maternal Cardiovascular Consequences of Pregnancy===
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| - | A. Cardiac out increases about one-third - comparable to slow walking
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| - | B. Supine position limits cardiac output: uterus presses on abdominal vena cava. Women usually learn to lie on their sides.
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| - | C. Heart rate steadily increases with fetal growth, but change should be small
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| - | D. Stroke volume first increases and then either levels off or lowers a bit. Heart rate increase over time maintains increased cardiac output
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| - | E. Mother's blood volume increases about 1 liter (25% for most women) and total body extracellular water increases 6-7 liters: Mom, baby, amniotic fluid
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| - | F. Total body red cell mass increases but hematocrit tends to decrease because plasma volume increases more than red cell mass.
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| - | G. Ideally, the mean arterial blood pressure should be relatively constant.
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| - | H. Increased cardiac output offset by lowered system vascular resistance (SVR): A new, large organ is forming plus heat dissipation by skin vasodilation is needed. At term pregnancy, uterus receives about 17-20% of cardiac output.
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| - | I. Gradual increase in SVR after 20 weeks is not well understood. Possibly due to stress of supporting the enlarging fetus?
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| - | J. Mother's oxygen consumption increases about 50% to support fetus and her increased cardiovascular performance, body mass, and renal function to clear fetal wastes.
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| - | ===IV. Circulatory changes at birth===
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| - | : The switch from placental to pulmonary vasculatures for gas exchange.
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| - | 1. When the lung expands with air, pulmonary vascular resistance dramatically decreases and allows increased blood flow.
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| - | 2. The ductus arterious closes as PGE2 decreases as the tissues become less hypoxic: also increased bradykinin may constrict
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| - | 3. Placental perfusion continues during birth process but stops once ventilation increases blood plasma oxygen. Placental vessels constrict to avoid fetal hemorrhage
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| - | 4. The decrease in pulmonary vascular resistance upon ventilation increases blood flow through right ventricle to lung. Lowers right atrial pressure and raises left atrial pressure such that foramen ovale flap mechanically seals and eventually anatomically fuses with atrial septum in >95% of humans.
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| - | 5. After birth occurs, fetal hemoglobin will be gradually replaced with the
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| - | adult form of hemoglobin .
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| - | 6. Pulmonary arterioles lose their heavy muscle layer which allows pulmonary vascular resistance to decrease
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| - | ===Clinical case===
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| - | A sustained pulsing murmur is heard in the upper chest of a 12 hour old full term neonate. The child is not cyanotic or hypoxic, but heart rate is high and arterial pressure is below normal. A probable diagnosis and treatment would be
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| - | *A. aortic valve incompetence requiring valve replacement/repair.
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| - | *B. open atrial septum defect requiring catheter placement of patch.
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| - | *C. mitral valve stenosis requiring valve replacement/repair.
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| - | *D. open ductus arteriosus treated with cycloxygenase blocking drug.
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| - | *E. coarctation of the ascending aorta requiring aortic resection.
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| - | ===Clinical case===
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| - | A 27 year old pregnant woman having her first child is seen for her
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| - | 36 week checkup. She is having light-headed episodes when lying down, particularly when trying to go to sleep at night. Her arterial pressure and heart rate while standing is 120/70 mmHg and 87 beats/min, sitting is 115/65 mmHg and 79 beats/min, and lying down is 90/50 mmHg and 107 beats/min. The most likely cause of the supine hypotension is
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| - | *A. failure of baroreceptor function.
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| - | *B. vena cava compression by the uterus/fetus.
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| - | *C. early heart failure due to pregnancy demands.
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| - | *D. relative hypovolemia for her stage of pregnancy.
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| - | *E. a pulmonary artery clot that blocks by body position.
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| - | *stopped here on 01/31/11 at 12PM.
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