The new 6-unit individualized curriculum for pediatric residents: the perspective of neonatology fellowship program directors.

OBJECTIVE: Starting in 2013, all pediatric residents entering fellowship must be provided six educational units whose structure is to be determined by their individual career plans. We sought to determine whether (1) neonatology fellowship program directors (PDs) consistently identify certain weaknesses among incoming fellows and (2) neonatology fellowship PDs agree on the most beneficial activities in which pediatric residents should participate to improve preparation for entry into neonatology fellowships. STUDY DESIGN: We sent a 21-question survey focused on the structure and implementation of the 6-unit curriculum to all members of the Organization of Neonatology Training Program Directors. RESULTS: Sixty-seven percent of PDs responded. Seventy-five percent cited insufficient procedural skills as the primary weakness of incoming fellows. More than 80% rated additional training in clinical neonatology, including procedural and resuscitation training, as 'beneficial' or 'highly beneficial'. In contrast, fewer than 40% of PDs gave the same positive ratings to activities broadly focused on scholarship. CONCLUSIONS: The results of the survey may help guide pediatric residency programs as they undertake development of these new curricular initiatives for individual residents entering neonatology.

Prostaglandin E2 decreases fetal breathing movements, but not pulmonary blood flow, in fetal sheep.

Fetal breathing movements are vital for normal fetal lung growth. Inhibition of these fetal breathing movements is associated with pulmonary hypoplasia. Pulmonary hypoplasia also occurs subsequent to alterations in other factors, such as a significant decrease in pulmonary blood flow. The prostaglandin system is known to have profound effects on both fetal breathing movements and on the pulmonary vascular system. We studied six late-gestation chronically instrumented fetal sheep by using an electromagnetic flow transducer around the left pulmonary artery to determine whether a decrease in fetal breathing movements, subsequent to a continuous infusion of prostaglandin E2 (PGE2), is associated with a decrease in pulmonary blood flow. A continuous PGE2 infusion of 0.88 +/- 0.11 microgram.kg-1.min-1 over 120 min led to a significant decrease in fetal breathing movements (control 40.5 +/- 3.6%, infusion 3.3 +/- 1.6%; P < 0.001). In contrast, the PGE2 infusion had no effect on mean left pulmonary artery blood flow (control 27.7 +/- 9.3 ml.min-1.kg-1, infusion 23.8 +/- 7.0 ml.min-1.kg-1. The PGE2 infusion demonstrated central effects in the percentage of time the fetus was in high-voltage electrocortical activity (control 41.9 +/- 2.5%, infusion 56.5 +/- 5.4%; P < 0.05) and in the amount of time spent in low-voltage electrocortical activity without fetal breathing movements (control 17.5 +/- 2.7%, infusion 40.2 +/- 4.8%; P < 0.05). A significant decrease in the fetal heart rate during the infusion was seen with no effect on either the systemic or pulmonary blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of inhibition of prostaglandin synthesis on breathing movements and pulmonary blood flow in fetal sheep.

During transition from fetal to extrauterine life, respiration increases in incidence and magnitude as pulmonary blood flow dramatically increases. To determine whether alterations in pulmonary blood flow in utero are directly related to alterations in fetal breathing movements (FBM), we studied six chronically instrumented fetal sheep late in gestation to assess the effects of continuous FBM caused by a 4-h infusion of meclofenamate, a prostaglandin synthase inhibitor, on mean pulmonary blood flow to the fetus. We found a striking increase in FBM from 46 +/- 15% (SD) of the time during control to > 85% of the time by 1 h (P < 0.001), with the fetuses exhibiting continuous FBM by the last 1 h of infusion. The mean pulmonary blood flow also increased significantly during the first 90 min of the infusion as the incidences of FBM were increasing (26 +/- 14 and 56 +/- 23 ml.min-1.kg-1 for control and infusion, respectively; P < 0.01). Despite the simultaneous initial increase in FBM and mean pulmonary blood flow, the increase in left pulmonary artery blood flow was not sustained and decreased back to baseline by 2 h, even though the incidence of FBM continued to increase at this time. During the infusion, the mean pulmonary blood flow was not different between the presence or absence of FBM. There were no changes in fetal heart rate or pulmonary or systemic blood pressures during the infusion nor in arterial pH or blood gas tensions. We conclude that this increase in mean pulmonary blood flow in utero was not solely related to the increase in breathing movements.

The effect of fetal breathing movements on pulmonary blood flow in fetal sheep.

In the fetus, normal lung growth requires both fetal breathing movements (FBM) and adequate pulmonary blood flow. We postulated that FBM intermittently increase pulmonary blood flow and may stimulate lung growth through that effect. To test the hypothesis that normal intermittent FBM cause associated intermittent increases in pulmonary blood flow, we studied eight chronically instrumented fetal sheep (gestational ages 125-143 d) on 34 occasions (total study time = 65.7 h). Each fetus had a cuff electromagnetic flow transducer around the left pulmonary artery, electrocortical electrodes, and catheters in the trachea, main pulmonary artery, carotid artery, and amniotic cavity. Mean blood flow though the left pulmonary artery averaged 59 +/- 8 mL/min (mean +/- SEM; per kg: 25 +/- 4 mL/kg/min) and was similar in both the presence (61 +/- 9 mL/min) and absence (57 +/- 7 mL/min) of FBM and during both high and low voltage electrocortical activity. In contrast, in utero phasic pulmonary blood flow varied with FBM, increasing during the inspiratory phase and decreasing during the expiratory phase. Both pulmonary and systemic vascular pressures showed changes in the opposite directions. Arterial pH and blood gas tensions were normal and did not change with FBM or electrocortical activity. We conclude that FBM do not increase mean blood flow through the left pulmonary artery; thus, it is unlikely that FBM stimulate lung growth through changes in pulmonary blood flow.

Effects of acute oligohydramnios on respiratory system of fetal sheep.

Prolonged oligohydramnios, or a lack of amniotic fluid, is associated with pulmonary hypoplasia and subsequent perinatal morbidity, but it is unclear whether short-term or acute oligohydramnios has any effect on the fetal respiratory system. To investigate the acute effects of removal of amniotic fluid, we studied nine chronically catheterized fetal sheep at 122-127 days gestation. During a control period, we measured the volume of fluid in the fetal potential airways and air spaces (VL), production rate of that fluid, incidence and amplitude of fetal breathing movements, tracheal pressures, and fetal plasma concentrations of cortisol, epinephrine, and norepinephrine. We then drained the amniotic fluid for a short period of time [24-48 h, 30.0 +/- 4.0 (SE) h] and repeated the above measurements. The volume of fluid drained for the initial studies was 1,004 +/- 236 ml. Acute oligohydramnios decreased VL from 35.4 +/- 2.9 ml/kg during control to 22.0 +/- 1.6 after oligohydramnios (P less than 0.004). Acute oligohydramnios did not affect the fetal lung fluid production rate, fetal breathing movements, or any of the other measured variables. Seven repeat studies were performed in six of the fetuses after reaccumulation of the amniotic fluid at 130-138 days, and in four of these studies the lung volume also decreased, although the overall mean for the repeat studies was not significantly different (27.0 +/- 5.2 ml/kg for control vs. 25.5 +/- 5.5 ml/kg for oligohydramnios). Again, none of the other measured variables were altered by oligohydramnios in the repeat studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Meclofenamate increases ventilation in lambs.

To investigate the effects of the prostaglandin synthetase inhibitor, meclofenamate, on postnatal ventilation, we studied 11 unanaesthetised, spontaneously-breathing lambs at an average age of 7.9 +/- 1.1 days (SEM; range 5-14 days) and an average weight of 4.9 +/- 0.5 kg (range 3.0-7.0 kg). After a 30-min control period we infused 4.23 mg/kg meclofenamate over 10 min and then gave 0.23 mg/h per kg for the remainder of the 4 h. Ventilation increased progressively from a control value of 515 +/- 72 ml/min per kg to a maximum of 753 +/- 100 ml/min per kg after 3h of infusion (P less than 0.05) due to an increased breathing rate; the effects were similar during both high- and low-voltage electrocortical activity. There were no significant changes in tidal volume, heart rate, blood pressure, arterial pH or PaCO2, the increased ventilation resulted from either an increase in dead space ventilation or an increase in CO2 production. This study indicates that meclofenamate causes an increase in ventilation in lambs but no changes in pH of PaCO2. The mechanism and site of action remain to be defined.

Intravenous lipid and amino acids briskly increase plasma glucose concentrations in small premature infants.

We determined the glycemic response to intravenous lipid infusion alone, lipid with amino acids, or amino acids alone in 15 very small premature infants receiving constant glucose infusion during early life. Infants who received lipid or lipid and amino acids demonstrated significant increases in glucose compared with infants who received amino acids. The combination of lipid and amino acids resulted in an earlier increase than lipid alone. Although plasma insulin did not change in all three groups, infants who received amino acids alone demonstrated an appropriate increase in glucagon. These data suggest that lipid infusion, a commonly used means of providing nutrition to premature infants, may cause significant disturbances in glucoregulation, particularly when administered with amino acids.

Prostaglandin E2 causes hypoventilation and apnea in newborn lambs.

To test the hypothesis that prostaglandin (PG) E2 is a respiratory depressant in the newborn lamb, 12 chronically catheterized, unanesthetized lambs (age 2-6 days) were infused with progressively increasing doses of PGE2 (0.1, 0.5, 1.0, and 5.0 micrograms.kg-1.min-1; 30 min for each dose) into the ascending aorta. PGE2 caused significant progressive decreases in ventilation (due to decreased tidal volume and breathing rate), heart rate, blood pressure, and percent of the time spent in low-voltage electrocortical activity (LVA). PGE2 also caused respiratory acidosis, hypoxemia, and increased frequency and duration of apneic events (greater than 3 s). During the infusion there was a dose-related increase in plasma concentration of PGE2. At 30 min postinfusion, all measured variables showed recovery, although arterial pH, CO2 tension, and plasma PGE2 remained significantly different from control values, and the percent time in LVA was even higher than during control. Infusion of the vehicle alone (n = 5) caused no significant changes in any of the measured variables. The results, taken in combination with previous fetal studies, indicate that PGE2 has marked inhibitory effects on breathing movements both before and after birth.