Distribution of spectral energy on the body surface: a physiological road map to improve identification of patients vulnerable to sustained ventricular arrhythmias.
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Biomedical subjects
Publications and source records attributed to M E Caine.
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Maternal anti-Kell antibody was found in 127 of 127,076 pregnancies during a 16-year period (0.1%). Thirteen Kell-sensitized pregnancies ended with a Kell-positive newborn infant, five of these had a poor perinatal outcome (hydrops, intrauterine or neonatal death, hemoglobin less than 7.9 gm, congestive heart failure). Mothers with Kell-positive infants and poor outcome had anti-Kell titers greater than or equal to 1:128 at delivery. With a maternal anti-Kell titer less than 1:32 at delivery, only one baby was Kell positive and mildly affected by hemolytic disease. Spectrophotometric analysis of amniotic fluid (delta optical density at 450 nm) in three of four pregnancies with poor perinatal outcomes revealed values of delta optical density at 450 nm in the high midzone of Liley within 1 week of delivery. Therefore, Kell-sensitized patients have to be managed differently from patients with rhesus sensitization. A management scheme to optimize perinatal outcome in Kell-sensitized pregnancy is described on the basis of this largest reported series of Kell-sensitized pregnancies.
We evaluated the effects of alterations in fetal hematocrit on fetal oxygenation in 10 chronically catheterized fetal lambs. Hematocrit was varied from 10% to 55% by slow isovolemic exchange transfusions with plasma or packed red blood cells obtained freshly from donor fetuses. At each hematocrit studied, we measured umbilical blood flow (Qumb) and the oxygen concentrations in umbilical venous blood (CUVO2) and arterial blood (CAO2) and calculated fetal oxygen delivery (Qumb X CUVO2), oxygen extraction [(CUVO2 - CAO2)/CUVO2], and oxygen consumption [Qumb (CUVO2 - CAO2)]. Fetal oxygen delivery was maximal at a fetal hematocrit of 33% (mean oxygen delivery = 23 ml of oxygen per minute per kilogram of fetus) and decreased as hematocrit was raised or lowered from that value. Despite these reductions in oxygen delivery, fetal oxygen consumption was relatively stable (at about 7 ml of oxygen per minute per kilogram) at hematocrits ranging from about 16% to 48% because of compensatory increases in fetal oxygen extraction. Regardless of whether oxygen delivery decreased because of anemia or polycythemia, fetal oxygen consumption was maintained as long as oxygen delivery was greater than about 14 ml of oxygen per minute per kilogram of fetus. When oxygen delivery was less than 14 ml of oxygen per minute per kilogram, fetal oxygen consumption fell while arterial blood base deficit increased, indicating that oxygen supply was inadequate for fetal oxygen demands. These results indicate that fetal aerobic metabolism can be sustained over a wide range of fetal hematocrits. Furthermore, our data support the concept that the level of fetal oxygen delivery is an important determinant of the adequacy of fetal oxygenation.