Objectives-To document the incidence, timing, degree, and associations of systemic hypoperfusion in the preterm infant and to explore the temporal relation between low systemic blood flow and the development of intraventricular haemorrhage (IVH). Study design-126 babies born before 30 weeks' gestation (mean 27 weeks, mean body weight 991 g) were studied with Doppler echocardiography and cerebral ultrasound at 5, 12, 24, and 48 hours of age. Superior vena cava (SVC) flow was assessed by Doppler echocardiography as the primary measure of systemic blood flow returning from the upper body and brain. Other measures included colour Doppler diameters of ductal and atrial shunts, as well as Doppler assessment of shunt direction and velocity, and right and left ventricular outputs. Upper body vascular resistance was calculated from mean blood pressure and SVC flow. Results-SVC flow below the range recorded in well preterm babies was common in the first 24 hours (48 (38%) babies), becoming significantly less common by 48 hours (6 (5%) babies). These low flows were significantly associated with lower gestation, higher upper body vascular resistance, larger diameter ductal shunts, and higher mean airway pressure. Babies whose mothers had received antihypertensives had significantly higher SVC flow during the first 24 hours. Early IVH was already present in 9 babies at 5 hours of age. Normal SVC flows were seen in these babies except in 3 with IVH, which later extended, who all had SVC flow below the normal range at 5 and/or 12 hours. Eight of these 9 babies were delivered vaginally. Late IVH developed in 18 babies. 13 of 14 babies with grade 2 to 4 IVH had SVC flow below the normal range before development of an IVH. Two of 4 babies with grade 1 IVH also had SVC flow below the normal range before developing IVH, and the other 2 had SVC flow in the low normal range. In all, IVH was first seen after the SVC flow had improved, and the grade of IVH related significantly to the severity and duration of low SVC flow. The 9 babies who had SVC flow below the normal range and did not develop IVH or periventricular leucomalacia were considerably more mature (median gestation 28 v 25 weeks).Conclusions-Low SVC flow may result from an immature myocardium struggling to adapt to increased extrauterine vascular resistances. Critically low flow occurs when this is compounded by high mean airway pressure and large ductal shunts out of the systemic circulation. Late IVH is strongly associated with these low flow states and occurs as perfusion improves. (Arch Dis Child Fetal Neonatal Ed 2000;82:F188-F194) Keywords: very preterm infants; blood flow; cerebral haemorrhage; superior vena cavaIn the beagle puppy model, intraventricular haemorrhage (IVH) is produced by inducing a severe hypoperfusion-reperfusion cycle.1 Our observations of early cardiovascular haemodynamics suggested that IVH in human preterm infants may relate to a similar cycle.2 3 Low ventricular outputs are common on day 1 in very preterm babies, subsequently improve...

One hundred and twenty ventilated preterm infants, birthweight <1500 g, were examined within the first 36 hours with colour Doppler echocardiography, to determine the cardiorespiratory influences on right (RVO) and left ventricular output (LVO). Forty nine of these infants had three further daily scans. Measurements included left ventricular (LV) ejection fraction, Doppler determination of RVO and LVO, and ductal and interatrial shunt direction, velocity and colour Doppler diameter. Infants were grouped by respiratory disease severity: mild, mean F102 in first 24 hours <0 5; moderate/severe, mean FI02 <05; and fatal, death resulting directly from acute respiratory distress.In the early studies ventricular outputs varied widely (RVO: 62-412 ml/kg/minute, LVO: 75-505 ml/kg/minute). The incidence of low ventricular outputs (<150 ml/kg/ minute) increased with worsening respiratory disease. The incidence of low RVO in the mild group was 19%, in the moderate/severe group 42%, and in the fatal group 85%. More infants had a low RVO than a low LVO, reflecting the impact of ductal shunting. Ductal and atrial shunting was predominantly left to right except in those with fatal respiratory disease. In those studied longitudinally, RVO and LVO increased with age and low outputs were not seen after day 3.Multilinear regression analyses, with RVO as the dependent variable, revealed increasing LVO and atrial shunt diameter as significant positive influences and increasing ductal shunt diameter and mean airway pressure as a significant negative influence. With LVO as the dependent variable, increasing RVO, ductal shunt diameter, and age were significant positive influences and increasing atrial shunt diameter was a significant negative influence.Low ventricular outputs are more common with worsening respiratory disease. Mean airway pressure and ductal shunting are two negative influences on ventricular outputs over which there is some therapeutic control.(Arch Dis Child 1996; 74: F88-F94) Keywords: cardiac output, ductus arteriosus, respiratory disease, Doppler echocardiography.A fundamental aim in intensive care of preterm infants is the maintenance of adequate and stable systemic and pulmonary perfusion. The haemodynamics of the preterm cardiovascular system are complex with the problems of the transitional circulation and changing pulmonary vascular resistance being compounded by an immature myocardium1 and shunting across the fetal channels of the ductus arteriosus and foremen ovale.2 3 Such shunting usually diverts blood left to right from the systemic back into the pulmonary circulation. For the ductus arteriosus, such shunting has been shown to 'steal' blood from the systemic circulation4; atrial shunting could have a similar effect. Occasionally these shunts are right to left and so divert blood from the pulmonary to the systemic circulation with resultant hypoxaemia. Positive pressure ventilation, often essential to maintain oxygenation, can also compromise cardiac output.5The output from each ventricle will refl...

While it is now recognized that umbilical cord clamping (UCC) at birth is not necessarily an innocuous act, there is still much confusion concerning the potential benefits and harms of this common procedure. It is most commonly assumed that delaying UCC will automatically result in a time-dependent net placental-to-infant blood transfusion, irrespective of the infant’s physiological state. Whether or not this occurs, will likely depend on the infant’s physiological state and not on the amount of time that has elapsed between birth and umbilical cord clamping (UCC). However, we believe that this is an overly simplistic view of what can occur during delayed UCC and ignores the benefits associated with maintaining the infant’s venous return and cardiac output during transition. Recent experimental evidence and observations in humans have provided compelling evidence to demonstrate that time is not a major factor influencing placental-to-infant blood transfusion after birth. Indeed, there are many factors that influence blood flow in the umbilical vessels after birth, which depending on the dominating factors could potentially result in infant-to-placental blood transfusion. The most dominant factors that influence umbilical artery and venous blood flows after birth are lung aeration, spontaneous inspirations, crying and uterine contractions. It is still not entirely clear whether gravity differentially alters umbilical artery and venous flows, although the available data suggests that its influence, if present, is minimal. While there is much support for delaying UCC at birth, much of the debate has focused on a time-based approach, which we believe is misguided. While a time-based approach is much easier and convenient for the caregiver, ignoring the infant’s physiology during delayed UCC can potentially be counter-productive for the infant.