Background Recent studies suggest that delayed cord clamping (DCC) is advantageous for achieving hemodynamic stability and improving oxygenation compared to the immediate cord clamping (ICC) during fetal-to-neonatal transition yet there is no quantitative information on hemodynamics and respiration, particularly for pre-term babies and fetal disease states. Therefore, the objective of this study is to investigate the effects of ICC and DCC on hemodynamics and respiration of the newborn preterm infants in the presence of common vascular pathologies. Methods A computational lumped parameter model (LPM) of the placental and respiratory system of a fetus is developed to predict blood pressure, flow rates and oxygen saturation. Cardiovascular system at different gestational ages (GA) are modeled using scaling relations governing fetal growth with the LPM. Intrauterine growth restriction (GR), patent ductus arteriosus (PDA) and respiratory distress syndrome (RDS) were modeled for a newborn at 30 weeks GA. We also formulated a “severity index ( SI )” which is a weighted measure of ICC vs. DCC based on the functional parameters derived from our model and existing neonatal disease scoring systems. Results Our results show that transitional hemodynamics is smoother in DCC compared to ICC for all GAs. Blood volume of the neonate increases by 10% for moderately preterm and term infants (32–40 wks) and by 15% for very and extremely preterm infants (22–30 wks) with DCC compared to ICC. DCC also improves the cardiac output and the arterial blood pressure by 17% in term (36–40 wks), by 18% in moderately preterm (32–36 wks), by 21% in very preterm (28–32 wks) and by 24% in extremely preterm (20–28 wks) births compared to the ICC. A decline in oxygen saturation is observed in ICC received infants by 20% compared to the DCC received ones. At 30 weeks GA, SI were calculated for healthy newborns (1.18), and newborns with GR (1.38), PDA (1.22) and RDS (1.2) templates. Conclusion Our results suggest that DCC provides superior hemodynamics and respiration at birth compared to ICC. This information will help preventing the complications associated with poor oxygenation arising in premature births and pre-screening the more critical babies in terms of their cardiovascular severity.

In Nature, there exist a variety of cardiovascular circulation networks in which the energetic ventricular load has both steady and pulsatile components. Steady load is related to the mean cardiac output (CO) and the haemodynamic resistance of the peripheral vascular system. On the other hand, the pulsatile load is determined by the simultaneous pressure and flow waveforms at the ventricular outlet, which in turn are governed through arterial wave dynamics (transmission) and pulse decay characteristics (windkessel effect). Both the steady and pulsatile contributions of the haemodynamic power load are critical for characterizing/comparing disease states and for predicting the performance of cardiovascular devices. However, haemodynamic performance parameters vary significantly from subject to subject because of body size, heart rate and subject-specific CO. Therefore, a 'normalized' energy dissipation index, as a function of the 'non-dimensional' physical parameters that govern the circulation networks, is needed for comparative/ integrative biological studies and clinical decision-making. In this paper, a complete network-independent non-dimensional formulation that incorporates pulsatile flow regimes is developed. Mechanical design variables of cardiovascular flow systems are identified and the Buckingham Pi theorem is formally applied to obtain the corresponding non-dimensional scaling parameter sets. Two scaling approaches are considered to address both the lumped parameter networks and the distributed circulation components. The validity of these non-dimensional number sets is tested extensively through the existing empirical allometric scaling laws of circulation systems. Additional validation studies are performed using a parametric numerical arterial model that represents the transmission and windkessel characteristics, which are adjusted to represent different body sizes and non-dimensional haemodynamic states. Simulations demonstrate that the proposed nondimensional indices are independent of body size for healthy conditions, but are sensitive to deviations caused by off-design disease states that alter the energetic load. Sensitivity simulations are used to identify the relationship between pulsatile power loss and non-dimensional characteristics, and optimal operational states are computed.

The transition from fetal to neonatal circulation requires a concert of events to transfer gas exchange function from the placenta to the lungs and separate the pulmonary and systemic pathways. Pulmonary vascular resistance (PVR) rapidly decreases within the first minutes of extrauterine life and continues to gradually decrease during the first week, increasing pulmonary blood flow and reducing pulmonary pressure [1, 2]. Umbilical vessels constrict, removing the placental circulation and leading to closure of the ductus venosus (DV) [2]. The increased left atrial filling and reduced right atrial filling results in permanent closure of the flap of the foramen ovale, removing the R→L interatrial shunt. Closure of the ductus arteriosus (DA) completes the separation of the pulmonary and systemic circulations by 48 hours in 82% of term newborns and by 96 hours in 100% [3]. Removal of the placental circulation is routinely achieved by umbilical cord clamping (UCC) immediately after birth. This practice, however, has been called into question by many studies, which suggest that continued umbilical flow in the early neonate is beneficial, and immediate UCC can lead to infant anemia [4, 5]. Due to routine UCC, the effects of this practice on transitional flow patterns are largely unknown [1, 6]. We therefore developed a lumped parameter model (LPM) to study the role of UCC in the fetal to neonatal transition. Our model includes time-varying resistance functions that allow us to simulate the opening of the PVR and closure of the DA and umbilical vessels. This model demonstrates that UCC can lead to an earlier onset of DA flow reversal and slightly reduced cardiac output (CO).