Early hemodynamic consequences of patent ductus arteriosus in preterm infants with intrauterine growth restriction.

OBJECTIVE: To test the hypothesis that significant patent ductus arteriosus (PDA) may occur very early after birth in preterm infants with intrauterine growth restriction (IUGR), we compared the longitudinal changes in left-to-right shunting through DA between eutrophic and preterm infants with IUGR. STUDY DESIGN: The preterm infants -26 to 32 weeks gestational age (GA), admitted in our neonatal intensive care unit from February to May 2004 were included. They were separated into an "IUGR of placental origin" group and an "eutrophic" group. Significant PDA was assessed by Doppler echocardiography at 6, 24, and 48 hours of age. RESULTS: Thirty-one eutrophic (GA = 29 +/- 1.4 weeks; birth weight [BW] = 1300 +/- 160 g) and 17 infants with IUGR (GA = 29.3 +/- 1.5 weeks; BW = 810 +/- 140 g) were studied. Six hours after birth, the rate of significant PDA was higher in the IUGR than in the eutrophic group (10/17 [60%] vs 5/31 [15%]; P < .05). More DA became significant in infants with IUGR (11/17 [65%]) than in eutrophic infants (12/31 [40%]) (P < .05) within the 48 hours after birth. CONCLUSION: Markers of high pulmonary blood flow and systemic vascular steal occur more frequently and earlier after birth in IUGR of placental origin than in eutrophic preterm infants. The management of preterm infants with severe IUGR of placenta origin should include early echocardiographic monitoring to assess for markers of significant PDA.

Dynamic behavior of respiratory system during nasal continuous positive airway pressure in spontaneously breathing premature newborn infants.

The end-expiratory lung-volume level of premature newborn infants is maintained above passive resting volume during active breathing, through the combination of reduced time constant and high respiratory rate. To determine whether nasal continuous positive airway pressure (NCPAP) alters this characteristic dynamic breathing pattern, we studied the effects of various NCPAP levels on the dynamic elevation of end-expiratory lung volume level (DeltaEELV) in spontaneously breathing premature newborn infants, using respiratory inductive plethysmography (RIP). Eleven premature newborn infants with moderate respiratory failure were included. NCPAP levels were set in a random order to 0, 2, 4, and 6 cm H2O. Tidal volume (Vt), rib-cage contribution to Vt (%RC), phase angle between abdominal and thoracic motions (theta), respiratory rate (RR), and inspiratory and expiratory times (Ti and Te) were continuously recorded by RIP. The slope of the linear part of the expiratory flow-volume relation was extrapolated up to zero flow level to evaluate the dynamic elevation of the functional residual capacity (FRC) (DeltaEELV). The time-constant of the respiratory system (tauRS) was calculated as the slope of the linear part of the expiratory flow-volume loop. At NCPAP = 6 cm H2O, DeltaEELV reached 0.6 +/- 0.2 times the Vt at NCPAP = 0 cm H2O. An increase in NCPAP level resulted in a significant decrease in DeltaEELV (P < 0.01). A decrease in DeltaEELV during NCPAP was associated with a significant increase in Te from 0.62 +/- 0.13 sec at NCPAP = 0 cm H2O to 0.80 +/- 0.07 sec at NCPAP = 6 cm H2O (P < 0.05), and a decrease in tauRS from 0.4 +/- 0.1 sec at NCPAP = 0 cm H2O to 0.24 +/- 0.04 sec at NCPAP = 6 cm H2O (P < 0.01). These results indicate that the characteristic spontaneous breathing pattern causing a dynamic elevation of FRC is abolished by NCPAP. We speculate that the dynamic volume-preserving mechanisms resulting from expiratory flow braking are no longer required during NCPAP, as the constant pressure may passively elevate FRC.

Effects of antenatal glucocorticoids on circulatory adaptation at birth in the ovine fetus.

OBJECTIVE: Adaptation to extra-uterine life requires dramatic increase in pulmonary blood flow. Mechanisms that induce pulmonary vasodilatation at birth are incompletely understood but include alveolar ventilation, increase in PaO2, and production of vasoactive mediators. We hypothesized that antenatal glucocorticoids (GC) increase pulmonary vasodilatation to birth-related stimuli. STUDY DESIGN: To test this hypothesis, we studied the pulmonary hemodynamic response at birth to mechanical ventilation with low (<10%) and then with high (100%) FiO2 in chronically prepared late-gestation fetal lambs treated or not by antenatal maternal steroids. RESULTS: Basal mean aortic and pulmonary artery pressure (PAP), left pulmonary blood flow, pulmonary vascular resistance (PVR), and blood gas were similar between control and dexamethasone-treated animals (GC group). During mechanical ventilation with low FiO2, mean PVR decreased by 40% in the control group (from 0.44 +/- 0.01 to 0.25 +/- 0.01 mm Hg/ml/min) and by 60% in the GC group (from 0.44 +/- 0.02 to 0.19 +/- 0.02 mm Hg/ml/min) (p < 0.01). When subsequently ventilated with 100% O2, there was no difference in PVR decrease between groups (0.15 +/- 0.02 mm Hg/ml/min in the GC group vs. 0.14 +/- 0.01 mm Hg/ml/min in the control group). CONCLUSION: Antenatal GC enhance pulmonary vasodilatation induced by alveolar ventilation at birth but do not alter the pulmonary vascular response to O2. We speculate that antenatal steroids exposure improve adaptation at birth through acceleration of both parenchymal and vascular lung maturation.