Relationship Between Blood Pressure, Cerebral Electrical Activity, Cerebral Fractional Oxygen Extraction, and Peripheral Blood Flow in Very Low Birth Weight Newborn Infants

Abstract

There is uncertainty about the level of systemic blood pressure required to maintain adequate cerebral oxygen delivery and organ integrity. This prospective, observational study on 35 very low birth weight infants aimed to determine the mean blood pressure (MBP) below which cerebral electrical activity, peripheral blood flow (PBF), and cerebral fractional oxygen extraction (CFOE) are abnormal. Digital EEG, recorded every day on the first 4 d after birth, were analyzed a) by automatic spectral analysis, b) by manual measurement of interburst interval, and c) qualitatively. CFOE and PBF measurements were performed using near-infrared spectroscopy and venous occlusion. MBP was measured using arterial catheters. The median (range) of MBP recorded was 32 mm . The EEG became abnormal at MBP levels below 23 mm Hg: a) the relative power of the delta (0.5-3.5 Hz) frequency band was decreased, b) interburst intervals were prolonged, and c) all four qualitatively abnormal EEG (low amplitude and prolonged interburst intervals) from four different patients were recorded below this MBP level. The only abnormally high CFOE was measured at MBP of 20 mm Hg. PBF decreased at MBP levels between 23 and 33 mm Hg. None of the infants in this study developed cystic periventricular leukomalacia. One infant (MBP, 22 mm Hg) developed ventricular dilatation after intraventricular hemorrhage. The EEG and CFOE remained normal at MBP levels above 23 mm Hg. It would appear that cerebral perfusion is probably maintained at MBP levels above 23 mm Hg. (Pediatr Res 59: 314-319, 2006) S everal authors have described an association between systemic hypotension in premature infants and neurologic morbidity (1-3), and, in some centers, clinical practice is to support blood pressure by inotropes and volume expanders when the MBP level falls below 30 mm Hg. The likely mechanism by which hypotension causes neurologic damage is by diminished oxygen delivery through decreased cerebral perfusion. However, the relationship between MBP and cerebral blood flow is unclear in premature infants (4 -8). Some authors have argued that cerebral blood flow is pressure passive and dependent on MBP in infants between 28 and 39 wk gestation (5,7). Others, who have studied infants between 24 and 34 wk gestation, observed that cerebral blood flow is independent of MBP (4,8). Furthermore, the critical level of MBP at which cerebral perfusion becomes compromised has not been clearly determined.In spite of a lack of evidence linking systemic hypotension to brain damage in very low birth weight infants, it is well known that older subjects lose consciousness when MBP falls to a seriously low level. A change in the level of consciousness may not be recognized in sick newborn infants who are heavily sedated while being ventilated, but it may be associated with recognizable changes in the EEG pattern. Using a cerebral function monitor, Greisen et al. (9) showed that reduced blood flow to the neonatal brain correlated with decreased amplitude of the EEG. There have bee...

Definition of hypotension and assessment of hemodynamics in the preterm neonate

“…11 The mean blood pressure value at which this occurs in the very preterm infant is unknown but may be near 24 mm Hg during the initial postnatal days. [23][24][25] Finally, if blood pressure continues to fall, structural integrity of the brain tissue will eventually be compromised ('ischemic blood pressure threshold', Figure 1). 11 In animal models, the ischemic blood pressure threshold is reached when the corresponding CBF is approximately 50% of the resting CBF.…”

Effect of permissive hypercapnia on background cerebral electrical activity in premature babies

“…Prolonged EEG IBIs of more than 30 s in preterm infants born at less than 28 wk gestation and more than 25 s in preterm infants born at more 28 wk gestation have been associated with increased incidence of death or developmental motor abnormalities (6,7). EEG has been studied in relation to age, hypotension, hypo and hypercapnia, and cardiac output in preterm babies born before 30 wk gestation during the first 72 h after birth (8)(9)(10)(11). Lower levels of blood carbon dioxide have been associated with slowing of cerebral electrical activity and increased cerebral fractional oxygen extraction, while hypercapnia was associated with suppression of cerebral electrical activity during the first 48 h after birth (9).…”

Diagnosis and treatment of the hypotensive very low birth weight infant during postnatal transition

“…5 Another approach to defining hypotension in VLBW neonates relies on assessing the changes in cerebral function and/or perfusion at different arterial pressure values. [6][7][8][9] A recent study has demonstrated that changes in brain electrical activity occur when mean arterial pressure drops below 24 mm Hg in the <4-day-old VLBW neonate. 6 However, the findings on the relationship between cerebral perfusion and arterial pressure are contradictory, as some studies found an association between low arterial pressure and cerebral hypoperfusion 6-8 while others did not.…”

“…[6][7][8][9] A recent study has demonstrated that changes in brain electrical activity occur when mean arterial pressure drops below 24 mm Hg in the <4-day-old VLBW neonate. 6 However, the findings on the relationship between cerebral perfusion and arterial pressure are contradictory, as some studies found an association between low arterial pressure and cerebral hypoperfusion 6-8 while others did not. 9 Thus, the lower limit of normal arterial pressure in the 1-day-old immature neonate remains to be determined.…”

“…11 Thus, as long as the fetal channels are open, left-to-right shunting will dominate even the early circulatory pattern of the VLBW infant and potentially result in pulmonary overcirculation and an inability to accurately assess systemic perfusion by measuring left cardiac output. To circumvent this problem, a series of recent studies used superior vena cava (SVC) flow [12][13][14] and near infrared spectroscopy 6,7,[15][16][17] to assess systemic perfusion and cerebral blood flow and oxygenation, respectively. The findings of these studies have shed light on the complexity of the transitional circulation and the impact of the initial systemic hypoperfusion on mortality and morbidity in the VLBW neonatal patient population.…”