Cerebral Autoregulation Dynamics in Premature Newborns

Panerai, Ronney B.; Kelsall, AW; Rennie, Janet M.; Evans, David H.

doi:10.1161/01.str.26.1.74

Cited by 104 publications

(76 citation statements)

References 21 publications

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“…An explanation for this aberrant result could neither be found during that experiment nor at postmortem autopsy, but as autoregulatory patterns, although slightly impaired in two animals, were found in the seven other animals, we conclude that this experimental model enables repeated valid assessments of cerebrovascular autoregulation. Even including this nonautoregulating animal the values of mean static autoregulatory response was well below the proposed thresholds of impaired autoregulation of 0.5 and 1.5% changes in CBF per mmHg change in MAP previously reported to indicate impaired cerebrovascular autoregulation in humans (18,19).…”

Section: Effects On Cerebrovascular Autoregulationcontrasting

confidence: 62%

Racemic ketamine does not abolish cerebrovascular autoregulation in the pig

Schmidt

Ryding

Åkeson

2003

Acta Anaesthesiol Scand

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Background: Little is known about the influence of racemic ketamine on autoregulation of cerebral blood flow (CBF), and available reports regarding its influence on cerebral hemodynamics are contradictory. This study was designed to evaluate cerebrovascular responses to changes in the mean arterial pressure (MAP) during ketamine anesthesia. Methods: In eight normoventilated pigs anesthesia was induced with propofol and maintained by i.v. infusion of ketamine (15.0 mg kg À1 .h À1 ) during measurements. The intra-arterial xenon clearance technique was used to calculate CBF. Balloon-tipped catheters were introduced in the inferior caval vein and mid-aorta, and increases or decreases by up to 40% in mean arterial pressure (MAP) in random order were achieved by titrated inflation of these balloon catheters. Cerebral blood flow was determined at each MAP level. Regression coefficients of linear pressure-flow curves were calculated in all animals. Results: From the mean baseline level (101 mmHg) MAP was reduced by 20% and 40%, and increased by 26% and 43%. The maximal mean increase and decrease in MAP induced a 12% increase and a 15% decrease, respectively, of CBF from the

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Section: Effects On Cerebrovascular Autoregulationcontrasting

confidence: 62%

Racemic ketamine does not abolish cerebrovascular autoregulation in the pig

Schmidt

Ryding

Åkeson

2003

Acta Anaesthesiol Scand

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“…Birth stress may have abolished cerebral autoregulation during hemorrhagic hypotension in the 127-d lambs in our study. This observation is supported by the observed failure of cerebral autoregulation in some studies in preterm-born humans (36,37). However, Tsuji et al (38) showed evidence of impaired autoregulation only in a subgroup of preterm infants who are at risk for developing germinal matrix-intraventricular hemorrhage and periventricular leukomalacia, whereas Tuszczuk et al (39) Brain cell function was preserved at MABP levels below the threshold value for maintenance of Qcar in the 141-d lambs.…”

Section: Discussionmentioning

confidence: 89%

Cerebral O2 Supply Thresholds for the Preservation of Electrocortical Brain Activity During Hypotension in Near-Term-Born Lambs

Os¹,

Liem²,

Hopman³

et al. 2005

Pediatr Res

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The fetal brain develops rapidly during the last trimester of pregnancy. Therefore, the brain of infants who are born preterm is vulnerable to changes in oxygen and nutrient supply in the neonatal period. The objective was to determine the effect of gestational age (GA) on the cerebral O 2 supply threshold level for preservation of brain function during hypotension in nearterm-born lambs. Lambs were delivered at 141 or 127 d of gestation Approximately 2% of all newborns in the Netherlands are born before 32 completed weeks of gestation. Although mortality rates have decreased over the past 15 y, long-term morbidity has not changed (1). Because the fetal brain develops very rapidly during the last trimester of pregnancy, the brain of infants who are born preterm is very vulnerable to changes in oxygen and nutrient supply in the neonatal period.Brain cells need a sufficient amount of oxygen for function, growth, and development. Cerebral O 2 supply is determined by the arterial oxygen content (CaO 2 ) and cerebral blood flow (CBF). If cerebral autoregulation is impaired, then hypotension results in low CBF and leads to decreases in cerebral O 2 supply. When cerebral O 2 supply becomes insufficient to meet the cellular demand for oxygen, a sequence of events will be triggered, eventually leading to neonatal brain cell dysfunction or damage.EEG features provide information on brain cell function (2). Energy failure in the brain, e.g. as a result of reduced cerebral O 2 supply during hemorrhagic hypotension, leads to a blockade of neuronal synaptic function and reduced electrical firing of neurons. A disadvantage of conventional EEG is that it requires the presence of an expert to interpret the large volumes of data. In an effort to solve this problem, various methods of compressing the EEG signal have been developed, the cerebral function monitor (CFM) being one of them. CFM correlates well with conventional multichannel EEG evaluation of cortical neuronal activity in neonates, except for the recognition of very short seizure activity patterns (3-8). Noninvasive recording of electrocortical brain activity (ECBA) by means of CFM-like signals can be used as a measure for brain cell function in the newborn period (2). Abnormal tracings are indicative of the risk for neonatal death and in the survivors to neurodevelopmental outcome (3,9 -12).

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“…Others have attempted to determine the status of cerebral autoregulation in premature infants by examining the slope (percentage change in CBF/1 mm Hg change in MABP) of the relationship between measurements of CBF and MABP (14,30,31). In addition to arbitrarily defining a critical value between 0.5 and 1.5% change in mCBFv/1 mm Hg change in MABP as intact autoregulation (30 -32), they did not take into account simultaneous changes in PaCO 2 that clearly cause changes in CBF and MABP in the same direction, which may be interpreted as impaired autoregulation.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Hypercapnia on Cerebral Autoregulation in Ventilated Very Low Birth Weight Infants

2005

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Permissive hypercapnia, a strategy allowing high PaCO 2 , is widely used by neonatologists to minimize lung damage in ventilated very low birth weight (VLBW) infants. While hypercapnia increases cerebral blood flow (CBF), its effects on cerebral autoregulation of VLBW infants are unknown. Monitoring of mean CBF velocity (mCBFv), PaCO 2 , and mean arterial blood pressure (MABP) from 43 ventilated VLBW infants during the first week of life was performed during and after 117 tracheal suctioning procedures. Autoregulation status was determined during tracheal suctioning because it perturbs cerebral and systemic hemodynamics. The slope of the relationship between mCBFv and MABP was estimated when PaCO 2 was fixed at 30, 35, 40, 45, 50, 55, and Neonatologists frequently use permissive hypercapnia, a strategy that allows high PaCO 2 (45-55 mm Hg), to avoid ventilator-induced lung injury during mechanical ventilation of premature infants (1). The theoretical benefit of permissive hypercapnia is that lower tidal volumes and mean airway pressures may prevent alveolar overdistension and lung injury (1). Randomized controlled trials of permissive hypercapnia, however, failed to demonstrate significant improvements in survival without chronic lung disease over routine ventilation strategies (1,2). Despite its widespread use, the effects of permissive hypercapnia on cerebral autoregulation of premature infants are not known.Cerebral autoregulation is an essential physiologic mechanism that maintains constant blood flow to the brain despite variations in cerebral perfusion pressure (3). The BP range over which CBF remains constant is known as the autoregulatory plateau. In this portion of the curve, CBF is independent of BP and the slope is 0. Below the autoregulatory plateau, CBF declines; above it, CBF rises in a pressure-passive manner (Fig. 1 A) (4,5). In contrast, in impaired autoregulation, CBF linearly follows changes in BP (over all BPs), where the slope is significantly Ͼ0 (Fig. 1B) (6). Despite the widespread belief that cerebral autoregulation is impaired in sick, ventilated premature infants (6), recent evidence using continuous monitoring systems suggests that many premature infants do have intact autoregulation (7,8

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Cerebral Autoregulation Dynamics in Premature Newborns

Cited by 104 publications

References 21 publications

Racemic ketamine does not abolish cerebrovascular autoregulation in the pig

Racemic ketamine does not abolish cerebrovascular autoregulation in the pig

Cerebral O2 Supply Thresholds for the Preservation of Electrocortical Brain Activity During Hypotension in Near-Term-Born Lambs

The Effects of Hypercapnia on Cerebral Autoregulation in Ventilated Very Low Birth Weight Infants

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