Biomedical subjects
Publications and source records attributed to R C Goodlin.
Severe edema-proteinuria-hypertension (EPH) gestosis (pre-eclampsia) appears in at least two forms (A and B). The A type is mostly complicated by fits, while the B type is characterized by multiple organ failure. The perinatal mortality rate is especially high in the B group. All gravid women with severe EPH gestosis benefit from blood volume expansion therapy.
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A gravida with severe hemoconcentration was studied with intravenous urography because of right upper quadrant pain. She subsequently developed renal failure. The potential hazard of urography in the presence of a severe blood volume contraction state is noted.
The case histories of 4 massively obese patients who underwent cesarean section are summarized. In all, a Pfannenstiel incision was made beneath the patient's huge panniculus, and a lower segment cesarean section was easily accomplished. There were no postoperative wound infections and all of the women had an essentially benign postoperative course.
We studied the effects of pharmacologic agents on umbilical blood flow and umbilical-placental vascular resistance in 18 fetal lambs in utero. Three groups of drugs were identified: the first had no effect on umbilical blood flow or umbilical-placental vascular resistance; the second altered umbilical blood flow secondary to changes in heart rate and placental perfusion pressure, but did not change umbilical-placental vascular resistance; the third decreased umbilical blood flow and increased umbilical-placental vascular resistance. The studies suggest mechanisms by which umbilical blood flow is regulated in the fetal lamb.
A case of diabetic acidosis during pregnancy is presented in which the fetal heart rate tracing demonstrated late decelerations. Sodium bicarbonate, intravenous fluids and insulin treatment resulted in correction of both the maternal acidosis and the abnormal fetal heart rate tracings. The rationale for bicarbonate therapy for treatment of the presumed fetal distress is discussed.
Acute and abrupt fetal bradycardia are considered to be vagal in origin. In addition to head compression and funis compression bradycardias, we will report on those acute fetal bradycardias occurring during maternal seizures and maternal voiding, during aortocaval compression, during terminal labor, and during the immediate postpartum period. While certain mechanisms are known which can explain some or parts of these bradycardias, we conclude that in the clinical setting information is insufficient to determine their etiology with precision. Instead of labeling abrupt fetal heart rate pattern as resulting from either head or funis compression, it is suggested that the patterns be described according to their severity and duration. Such acute fetal bradycardias can be detrimental in terms of reduced umbilical flow. Administration of atropine may be indicated in the otherwise healthy fetus with acute bradycardia.
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This review is designed to provide a broad view of fetal cardiovascular response to fetal distress. The presentation focuses on data obtained from laboratories working with fetal sheep, or occasionally fetal monkeys, instead of attempting to interpret data resulting from human fetal studies. Human fetal studies are unsatisfactory for any detailed analysis other than discussions of an occasional case history because of the difficulty of identifying controls and because cardiovascular experimentation is not ethically possible.
Twenty-eight women with severe pre-eclampsia were misdiagnosed and initially thought to have disorders unrelated to pregnancy. Their chief complaints included failing vision, liver or gallbladder dysfunction, renal failure, hemorrhage, seizures, and heart failure. Laboratory studies usually demonstrated thrombocytopenia and high hematocrit values. The development of these symptoms appears to begin with failure of the primigravida to appropriately increase her blood volume commensurate with the increase in size of her uterus. Expanding the severly pre-eclamptic patient's blood volume with intravenous albumin appears to be an effective and appropriate therapy.
The fetal heart rate recordings of 100 parturients given PCB with less than 200 mg. of lidocaine were reviewed. No PCB bradycardia occurred if there were no pre-PCB FHR decelerations (92 per cent accuracy). In an effort to prevent post-PCB bradycardia, atropine was given in the maternal paracervical area and also intravenously. The most effective dose was 1.0 mg. intravenously, but the prophylactic efficiency of atropine was uncertain in preventing the post-PCB bradycardia.
We studied the relationship of fetal and maternal vascular pressures to umbilical and uterine blood flow in the unanesthetized ewe and in the sheep fetus in utero by placing electromagnetic flow transducers around both the common umbilical and uterine arteries. Reductions in umbilical arterial pressure or elevations in umbilical venous pressure decreased umbilical blood flow without affecting either the uterine arterial blood flow or other maternal cardiovascular variables which were studied. Elevations in uterine venous pressure or reductions in uterine arterial pressure decreased uterine arterial flow but these interventions had no effect on umbilical blood flow until fetal hypoxemia and bradycardia occurred. When the bradycardia of the fetal hypoxic response was inhibited by atropine, alterations in maternal vascular pressure had no effect on umbilical arterial flow. These data do not support the presence of a "sluice" or "waterfall" effect in the umbilical-placental circulation of the sheep fetus in utero.
Intrauterine life demands unique respiratory and nutrient mechanisms, and it seems reasonable that some cardiorespiratory responses developed for later extrauterine life would not necessarily be entirely appropriate for the fetal period. In other words, a human fetus may not always be acting in its own best interest when it responds to intrauterine stress with what are appropriate extrauterine responses, such as gasping or the baroreflex (bradycardia). The detrimental effects of in utero gasping of meconium are well known, but the potentially harmful effects of inappropriate fetal bradycardia are little appreciated. A review of this condition is presented.