This study examined the relationships between cerebral fractional oxygen extraction (FOE), mean arterial blood pressure (MABP), left ventricular output (LVO), blood gases, and other physiologic variables in 36 very-low-birth-weight preterm infants during the first 3 d after birth. There was a decrease in cerebral FOE (p ϭ 0.008), and rises in LVO (p Ͻ 0.0001) and MABP (p ϭ 0.02) during the 3 d. Between d 1 and 2, cerebral FOE decreased (p ϭ 0.007) and LVO increased (p Ͻ 0.0001). There was no relationship between MABP and cerebral FOE. LVO correlated negatively with cerebral FOE on d 1 (p ϭ 0.01), but not on d 2 (p ϭ 0.07). On d 1, median pressure of arterial CO 2 was lower in infants with low LVO (Ͻ5 th centile) and high cerebral FOE (Ͼ95 th centile) than in infants with low LVO (Ͻ5 th centile) but normal cerebral FOE (5 th -95 th centile) (p ϭ 0.03). These findings suggest that cerebral FOE was increased only when LVO was low and there was hypocarbia. MABP had no demonstrable effect. It is likely that increased cerebral FOE is a normal physiologic response to maintain an adequate oxygen supply to the cerebral tissues when LVO is low and hypocarbia has caused vasoconstriction. It is possible that the cerebral hemispheres are low-priority vascular beds in the preterm infant, and that the high cerebral FOE is a result of reduced hemispheric blood flow to maintain MABP in the presence of low LVO. Acquired cerebral injury is a serious problem for infants born prematurely. The EPICure study, which examined the neurologic outcomes of infants born at 25 or fewer completed weeks of gestation, found that 49% of children had disability at a median age of 30 mo (corrected for gestation) (1). These children included 23% who met the criteria for severe disability. The two most common acquired cerebral lesions are intraventricular hemorrhage and cystic periventricular leukomalacia (2). Although both have a number of suggested etiologies, one commonly suggested factor is disturbed cerebral hemodynamics (3, 4). A number of studies have demonstrated that blood pressure may play an important role in the control of CBF and the pathogenesis of cerebral injury (4, 5). There is a widely held belief among clinicians that hypotension is an important cause of impaired organ perfusion, low CBF, insufficient cerebral oxygen delivery, and consequent cerebral injury, and considerable therapeutic effort is therefore put into maintaining blood pressure. This is in spite of several studies of the relationship between blood pressure and cerebral hemodynamics, which suggest that blood pressure may not be as important as it is currently thought to be (6 -10). There is, however, evidence that changes in blood gases, in particular changes in PaCO 2 , influence cerebral hemodynamics (11-13), with a probable link between hypocarbia and cerebral injury (14,15).Our own previous work has also failed to demonstrate any significant relationship between MABP and cerebral FOE (16). Cerebral FOE represents the ratio of oxygen consumption to delivery. As oxyg...

Cerebral blood flow (CBF) is known to be low in newborn infants, but this has not been shown to be damaging. The purpose of this study was to investigate the relationships between cerebral haemoglobin flow, blood flow, oxygen delivery, oxygen consumption, venous saturation, and fractional oxygen extraction (OEF) in newborn, preterm infants. Measurements were made by nearinfrared spectroscopy in 13 very preterm, extremely low birth weight infants (median gestation 25 weeks) during the first 3 days after birth. There was a negative correlation between cerebral oxygen delivery and OEF (n ¼ 13, r ¼ À0.5, P ¼ 0.03), which implies that when there is a reduction in cerebral oxygen delivery in sick preterm infants, increased cerebral oxygen extraction may be responsible for maintaining oxygen availability to the brain. During the first 3 days after birth CBF (n ¼ 13, r ¼ 0.7, P ¼ 0.01), oxygen delivery (n ¼ 13, r ¼ 0.5, P ¼ 0.03), and oxygen consumption (n ¼ 13, r ¼ 0.7, P ¼ 0.004) all increased. This increase in oxygen consumption indicates increased cerebral metabolic activity after birth, which is likely to be a normal adaptation to extrauterine life. The increases in blood flow and oxygen delivery may also be normal adaptations that facilitate this increase in metabolic activity. There was a decrease (P ¼ 0.04) in mean (7s.d.) cerebral OEF between day 1 (0.3770.10) and day 2 (0.2970.09), with no change between day 2 and day 3. Taking into account the negative correlation between OEF and oxygen delivery, this decrease in OEF may be because of increased oxygen delivery during this time.

Fluctuations in cerebral hemodynamics have been implicated in the pathogenesis of acquired brain damage in babies born prematurely. This study examined the changes in cerebral fractional oxygen extraction (FOE) over the first 3 d after birth in 25 verylow-birth-weight preterm infants. Twelve infants had no major cerebral injury and 13 had acquired brain injury; cystic periventricular leukomalacia (PVL) was present in 4 and intraventricular hemorrhage (IVH) in 9, of whom 2 also had hemorrhagic parenchymal infarction (HPI). Normal values (median, 5 th -95 th centiles) for cerebral FOE in very-low-birth-weight infants with no cerebral injury were 0. Cerebral white matter injury is responsible for considerable morbidity in infants born prematurely (1-5). The two principal underlying brain lesions are HPI and cystic PVL (6). Abnormal cerebral hemodynamics and oxygen delivery have been suggested as possible etiological factors for both lesions (7). Increased variability in cerebral blood flow or mean arterial blood pressure have been associated with the development of IVH (8 -11). By contrast, cystic PVL has been attributed to cerebral hypoperfusion (8,(12)(13)(14). Other studies, however, have demonstrated no relationship between the incidence of PVL and hypotension (15-17). There is also emerging evidence to implicate infection and inflammation, and the vulnerability of the oligodendrocyte precursors that inhabit the developing periventricular white matter, in the etiology of PVL (18 -24).Another variable that is related to cerebral perfusion and oxygen delivery is cerebral FOE, which represents the ratio of cerebral oxygen consumption to cerebral oxygen delivery. As oxygen delivery decreases, FOE would be expected to increase so that oxygen consumption remains constant. When oxygen delivery decreases beyond the critical point at which oxygen extraction is maximal and cannot increase further, oxygen consumption will start to decrease. This present study was undertaken to investigate the patterns of change in cerebral FOE over the first 3 d after birth in preterm, very-low-birthweight neonates, and to relate these changes to acquired cerebral injury. The hypothesis that was tested was that infants with no major cerebral injury would exhibit a different pattern of Received February 18, 2003; accepted September 9, 2003

This study examined the relationship between blood pressure, peripheral blood flow (PBF), and peripheral fractional oxygen extraction (FOE). Variables that may influence PBF and peripheral FOE were also measured. Measurements of PBF by near infrared spectroscopy and fractional shortening by echocardiography were made within 12 h of birth in 24 infants less than 32 wk gestation. Blood gases, Hb, temperature, and blood pressure were also measured. PBF was significantly correlated with fractional shortening (r ϭ 0.56, p ϭ 0.005), PO 2 (r ϭ Ϫ0.5, p ϭ 0.01), and peripheral temperature (r ϭ 0.52, p ϭ 0.01). Peripheral FOE was significantly correlated with fractional shortening (r ϭ Ϫ0.48, p ϭ 0.02), PO 2 (r ϭ 0.52, p ϭ 0.02), and PCO 2 (r ϭ Ϫ0.53, p ϭ 0.008), but not with peripheral temperature. There was no significant correlation between blood pressure and either PBF or peripheral FOE. These results indicate the importance of several physiologic variables, but not blood pressure, in determining peripheral tissue oxygen delivery in sick preterm infants receiving intensive care. It adds weight to the idea that blood pressure should not be considered a surrogate for peripheral blood flow and oxygen delivery. A dequate blood flow and oxygen delivery to the peripheral tissues of a sick, newborn infant is a sine qua non of neonatal intensive care. The adequacy of tissue oxygen delivery is difficult to measure directly, and thus it is usual to measure surrogate variables that may be related to tissue oxygen availability and are more amenable to continuous monitoring, such as arterial oxygen saturation and arterial blood pressure.Peripheral oxygen delivery is determined by peripheral blood flow (PBF) and arterial oxygen content. PBF is related to vascular resistance and blood pressure, which in turn depends on cardiac function; arterial oxygen content depends on the blood Hb concentration and arterial PO 2 .As blood flow is related to vascular resistance and blood pressure, there are a number of other factors that may influence blood flow and thus oxygen delivery to the peripheral tissues. These include blood gases, peripheral temperature, arterial Hb concentration, and cardiac function. During the first few hours after birth, which is a period of great instability for the critically ill preterm infant when blood pressure, left ventricular output and systemic blood flow are all low (1-3), PBF and thus oxygen delivery may be inadequate.Peripheral fractional oxygen extraction (FOE), the ratio of oxygen consumption to oxygen delivery (4), gives information on the adequacy of tissue oxygenation. Raised FOE most likely represents decreased oxygen delivery, which may be due to reduced blood flow (poor perfusion) or reduced arterial oxygen content (hypoxaemia).This study explored the relationships between physiologic variables and both PBF and peripheral FOE during the first 12 h after birth in a group of sick, ventilated, very low birth weight infants. The hypothesis tested was that PBF and peripheral FOE were correlate...