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Journal ArticleDOI

Impact of anesthetic agents on cerebrovascular physiology in children.

01 Feb 2009-Pediatric Anesthesia (Blackwell Publishing Ltd)-Vol. 19, Iss: 2, pp 108-118
TL;DR: The understanding of the effects of anesthetic agents on the physiology of cerebral vasculature in the pediatric population has significantly increased in the past decade allowing a more rationale decision making in anesthesia management.
Abstract: care to children with neurologic pathologies. The cerebral physiology is influenced by the developmental stage of the child. The understanding of the effects of anesthetic agents on the physiology of cerebral vasculature in the pediatric population has significantly increased in the past decade allowing a more rationale decision making in anesthesia management. Although no single anesthetic technique can be recommended, sound knowledge of the principles of cerebral physiology and anesthetic neuropharmacology will facilitate the care of pediatric neurosurgical patients.

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Journal ArticleDOI
TL;DR: There is no direct evidence in humans for propofol-induced neurotoxicity to the infant brain; however, current concerns of neuroapoptosis in developing brains induced by prop ofol persist and continue to be a focus of research.
Abstract: Propofol is an intravenous agent used commonly for the induction and maintenance of anesthesia, procedural, and critical care sedation in children. The mechanisms of action on the central nervous system involve interactions at various neurotransmitter receptors, especially the gamma-aminobutyric acid A receptor. Approved for use in the USA by the Food and Drug Administration in 1989, its use for induction of anesthesia in children less than 3 years of age still remains off-label. Despite its wide use in pediatric anesthesia, there is conflicting literature about its safety and serious adverse effects in particular subsets of children. Particularly as children are not “little adults”, in this review, we emphasize the maturational aspects of propofol pharmacokinetics. Despite the myriad of propofol pharmacokinetic-pharmacodynamic studies and the ability to use allometrical scaling to smooth out differences due to size and age, there is no optimal model that can be used in target controlled infusion pumps for providing closed loop total intravenous anesthesia in children. As the commercial formulation of propofol is a nutrient-rich emulsion, the risk for bacterial contamination exists despite the Food and Drug Administration mandating addition of antimicrobial preservative, calling for manufacturers’ directions to discard open vials after 6 h. While propofol has advantages over inhalation anesthesia such as less postoperative nausea and emergence delirium in children, pain on injection remains a problem even with newer formulations. Propofol is known to depress mitochondrial function by its action as an uncoupling agent in oxidative phosphorylation. This has implications for children with mitochondrial diseases and the occurrence of propofol-related infusion syndrome, a rare but seriously life-threatening complication of propofol. At the time of this review, there is no direct evidence in humans for propofol-induced neurotoxicity to the infant brain; however, current concerns of neuroapoptosis in developing brains induced by propofol persist and continue to be a focus of research.

256 citations


Cites background from "Impact of anesthetic agents on cere..."

  • ...This is associated with a fall in cerebral blood flow, metabolic demand for oxygen, and any pre-existing cerebral edema [88, 89]....

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Journal ArticleDOI
TL;DR: Near‐infrared spectroscopy provides noninvasive continuous access to the venous side of regional circulations that can approximate organ‐specific and global measures to facilitate the detection of circulatory abnormalities and drive goal‐directed interventions to reduce end‐organ ischemic injury.
Abstract: The safety of anesthesia has improved greatly in the past three decades. Standard perioperative monitoring, including pulse oximetry, has practically eliminated unrecognized arterial hypoxia as a cause for perioperative injury. However, most anesthesia-related cardiac arrests in children are now cardiovascular in origin, and standard monitoring is unable to detect many circulatory abnormalities. Near-infrared spectroscopy provides noninvasive continuous access to the venous side of regional circulations that can approximate organ-specific and global measures to facilitate the detection of circulatory abnormalities and drive goal-directed interventions to reduce end-organ ischemic injury.

96 citations

Journal ArticleDOI
TL;DR: The advantages of total intravenous anesthesia (TIVA) have emerged and driven change in practice as mentioned in this paper, and these advantages will justify why TIVA will supercede inhalational anesthesia in future pediatric anesthetic practice.
Abstract: Inhalational anesthesia has dominated the practice of pediatric anesthesia. However, as the introduction of agents such as propofol, short-acting opioids, midazolam, and dexmedetomidine a monumental change has occurred. With increasing use, the overwhelming advantages of total intravenous anesthesia (TIVA) have emerged and driven change in practice. These advantages, outlined in this review, will justify why TIVA will supercede inhalational anesthesia in future pediatric anesthetic practice.

72 citations

01 Jan 1995
TL;DR: In this paper, the effects of a high affinity gamma-aminobutyric acid (GABA)-benzodiazepine-receptor agonist (lorazepam) and an antagonist (flumazenil) in humans, using H2(15)O positron-emission tomography were studied.
Abstract: We studied the effects of a high-affinity gamma-aminobutyric acid (GABA)-benzodiazepine-receptor agonist (lorazepam) and an antagonist (flumazenil) in humans, using H2(15)O positron-emission tomography. Administration of lorazepam to healthy volunteers caused time- and dose-dependent reductions in regional cerebral blood flow and self-reported alterations in behavioral/mood parameters. Flumazenil administration reversed these changes. These observations indicated that benzodiazepine-induced effects on regional cerebral blood flow and mood/behavior are mediated at some level through GABA-benzodiazepine receptors, although the specific mechanism remains unclear. The approach described here provides a method for quantifying GABA-benzodiazepine-receptor-mediated neurotransmission in the living human brain and may be useful for studying the role of these receptors in a variety of neuropsychiatric disorders.

53 citations

References
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Journal ArticleDOI
TL;DR: It is concluded that nitrous oxide increases cerebral blood flow velocity in healthy children anaesthetised with 1.0 MAC sevoflurane.
Abstract: The aim of this study was to determine the effect of nitrous oxide on cerebral blood flow velocity in children anaesthetised with desflurane. Eighteen healthy children scheduled for elective surgery were enrolled into the study. Anaesthesia was induced using sevoflurane, and a caudal block was performed following tracheal intubation. Anaesthesia was maintained with 1 age-adjusted MAC desflurane. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Each patient was randomised to receive a sequence of either air/nitrous oxide/air or nitrous oxide/air/nitrous oxide in 30% oxygen. Fifteen minutes after each change in the nitrous oxide concentration, three measurements of cerebral blood flow velocity, blood pressure and heart rate were recorded. Neither the addition nor removal of nitrous oxide caused any significant changes in middle cerebral artery blood flow velocity, heart rate or blood pressure. This may be due to a more potent cerebral vasodilatory effect of desflurane in children.

25 citations

Journal ArticleDOI
TL;DR: It is suggested that nitrous oxide does not affect the dynamic cerebrovascular reactivity to acute arterial carbon dioxide (CO 2 ) changes, although it does produce a mild increase in normocapnic cerebral blood flow velocity.
Abstract: We sought to clarify the effect of nitrous oxide (N 2 O) on the immediate responses of cerebral vasculature to sudden changes in arterial carbon dioxide tension in healthy humans. By use of a transcranial Doppler ultrasonography, blood flow velocity in the middle cerebral artery (V MCA ) was measured during a step increase followed by a step decrease in end-tidal CO 2 tension (PETCO 2 ) between normo- and hypercapnia while subjects inspired gas mixtures containing 70% O 2 +30% N 2 (control) and 70% O 2 + 30% N 2 O (N 2 O) separately. During the control condition, both step increase and decrease in PETCO 2 produced rapid exponential changes in V MCA . An increase in V MCA produced by the step increase in PETCO 2 was smaller (P < 0.001) and slower (P <0.001) than a decrease in V MCA induced by the step decrease in PETCO 2 . These general features of the dynamic cerebrovascular response were not affected by substitution of N 2 O for N 2 in the inspired gases although N 2 O increased baseline V MCA by 15% (P < 0.001) compared with the control condition. We conclude that N 2 O in itself does not affect the dynamic cerebrovascular response to arterial CO 2 changes, although it produces static mild cerebral vasodilation. Implications: This study suggests that nitrous oxide does not affect the dynamic cerebrovascular reactivity to acute arterial carbon dioxide (CO 2 ) changes, i.e., exponential changes in cerebral blood flow in response to step changes in alveolar CO 2 tension, although it does produce a mild increase in normocapnic cerebral blood flow velocity.

24 citations

Journal ArticleDOI
TL;DR: A review of age-related differences in critical values of arterial oxygen tension, arterial carbon dioxide tension, systemic arterial pressure and cerebral perfusion pressure confirms that it is necessary to establish critical values in neonates and infants for each of these variables, as well as for any possible sympathetic nervous system influences on cerebral blood flow.
Abstract: Although much information is known about the factors controlling cerebral blood flow in the adult, there are significant physiological differences between the neonate, infant, and the adult. Therefore, it is not possible directly to transfer information concerning control of cerebral blood flow in the adult to the pediatric age population. A review of age-related differences in critical values of arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2), systemic arterial pressure and cerebral perfusion pressure (CCP) confirms that it is necessary to establish critical values in neonates and infants for each of these variables, as well as for any possible sympathetic nervous system influences on cerebral blood flow.

24 citations

Journal ArticleDOI
TL;DR: Fentanyl was more effective than remifentanil at preventing increases in CBFV during and immediately following laryngoscopy and tracheal intubation in children undergoing sevoflurane anesthesia.
Abstract: Controlling the cerebral and systemic hemodynamic responses to laryngoscopy and tracheal intubation may play a role in determining clinical outcome in pediatric neurosurgical patients. This study compared the effects of remifentanil and fentanyl on cerebral blood flow velocity (CBFV) and hemodynamic profile during laryngoscopy and tracheal intubation in children under sevoflurane anesthesia. Sixty healthy children aged two to six years undergoing dental surgery under general anesthesia were enrolled. Each child was randomly assigned to receive a remifentanil or fentanyl infusion, at a rate of 0.75, 1.0, or 1.5 μg·kg−1·min−1 after induction of anesthesia with 2% sevoflurane. Middle cerebral artery blood flow velocity was measured by transcranial Doppler (TCD) sonography Once a baseline set of hemodynamic variables and TCD measurements were recorded, the opioid infusion was started. Measurements were taken at two-minute intervals, starting four minutes prior to laryngoscopy until four minutes following naso-tracheal intubation. Remifentanil caused a more significant decrease in mean arterial pressure and CBFV prior to tracheal intubation than did fentanyl (P < 0.001). During laryngoscopy and for two minutes following tracheal intubation, CBFV increased in all remifentanil groups (P < 0.05), whereas it remained stable in all fentanyl groups. This study suggests that fentanyl was more effective than remifentanil at preventing increases in CBFV during and immediately following laryngoscopy and tracheal intubation in children undergoing sevoflurane anesthesia. Fentanyl also seemed to provide a more stable hemodynamic profile prior to laryngoscopy and tracheal intubation when compared to remifentanil.

22 citations

Journal ArticleDOI
TL;DR: Data strongly suggest that isoflurane and halothane in doses up to 1.0 MAC do not affect the cerebrovascular reactivity of the MCA to CO2 in anaesthetized, healthy children.
Abstract: To determine the effects of isoflurane and halothane on cerebrovascular reactivity to CO2, 30 children aged one to six years were anaesthetized with isoflurane or halothane in an air and oxygen mixture with an FIO2 of 0.3. The end-tidal concentrations (0.5 minimum alveolar concentration (MAC) or 1.0 MAC) of isoflurane or halothane were age-adjusted. After achieving a steady-state at both 0.5 MAC and 1.0 MAC isoflurane and halothane, the end-tidal carbon dioxide tension (PETCO2) was randomly adjusted to 20, 40, or 60 mmHg. Cerebral blood flow velocity (CBFV) and the cerebrovascular resistance index (RI+) in the middle cerebral artery (MCA) were measured by a transcranial Doppler monitor. Three measurements of CBFV and RI+ were obtained at each PETCO2 and isoflurane or halothane concentration. Any rise in the PETCO2 caused an increase in CBFV during both 0.5 MAC (r2 = 0.99 and 0.99) and 1.0 MAC (r2 = 0.96 and 0.95) isoflurane and halothane anaesthesia, respectively (P less than 0.05). The CBFV for isoflurane increased as PETCO2 increased from 20 to 60 mmHg for both 0.5 MAC and 1.0 MAC (P less than 0.05). The CBFV for halothane increased as PETCO2 increased from 20 to 40 mmHg for both 0.5 MAC and 1.0 MAC halothane (P less than 0.05), but did not change as PETCO2 increased from 40 to 60 mmHg for both 0.5 MAC and 1.0 MAC halothane. The RI+ showed an inverse relationship with CBFV at each PETCO2 for 0.5 MAC (r2 = 0.98 and 0.99) and 1.0 MAC (r2 = 0.76 and 0.53) isoflurane and halothane, respectively (P less than 0.05). The CBFV did not differ significantly between 0.5 and 1.0 MAC isoflurane and halothane at corresponding PETCO2 values. The cerebrovascular response to CO2 at 20 mmHg between 0.5 MAC and 1.0 MAC halothane was not significantly different. These data strongly suggest that isoflurane and halothane in doses up to 1.0 MAC do not affect the cerebrovascular reactivity of the MCA to CO2 in anaesthetized, healthy children.

22 citations