Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Jul 1998
Effect of nitrous oxide on cerebral blood flow velocity after induction of hypocapnia.
Hyperventilation may reverse increases in cerebral blood flow velocity caused by inhalation of nitrous oxide (N2O). This study sought to determine whether inhalation of 50% nitrous oxide after the induction of hyperventilation increases cerebral blood flow velocity as measured by transcranial Doppler ultrasonography. Seven volunteers breathed air/O2 through a modified Circle system at normocapnia followed by air/O2 with hyperventilation, and then N2O/O2 with hyperventilation. ⋯ Mean cerebral blood flow velocity decreased 34% with hyperventilation (38+/-4 cm/second versus 59+/-9 cm/second, p < 0.05) and returned to baseline with the addition of nitrous oxide (58+/-7 cm/second), despite persistent hypocapnia. The addition of nitrous oxide to the inspired gas mixture after induction of hypocapnia reversed reductions in cerebral blood flow velocity associated with hyperventilation. Potential benefits of induced hypocapnia in patients with intracranial pathology may be offset by the administration of N2O.
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J Neurosurg Anesthesiol · Jul 1998
Case Reports Comparative StudyMalignant cerebral edema in patients with hypertensive intracerebral hemorrhage associated with hypertonic saline infusion: a rebound phenomenon?
Hypertonic saline was recently introduced as a new hyperosmolar agent for treatment of intracranial hypertension and cerebral edema. It has the potential to cause a rebound phenomenon similar to other osmotic agents. The authors report on two patients with cerebral edema caused by hypertensive intracerebral hemorrhage who were treated with hypertonic saline infusion. ⋯ Compared with pre-treatment computed tomographic scans, edema volume on repeat scans increased from 131 cc to 262 cc, and from 171 cc to 239 cc in the first and second patients, respectively, despite the lack of change in hematoma volume. Malignant edema formation late in the course of intracerebral hemorrhage after prolonged administration of hypertonic saline may represent a rebound phenomenon of hyperosmolar therapy. Further studies are warranted to identify the occurrence of this phenomenon and the subset of patients susceptible to it.
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J Neurosurg Anesthesiol · Jul 1998
Comparative StudyThe effects of exogenous epinephrine on a convulsive dose of lidocaine: relationship with cerebral circulation.
In order to understand why exogenous epinephrine decreases the convulsive dose of lidocaine, the authors investigated cerebral circulation and plasma lidocaine concentrations in Wistar rats under general anesthesia. In the first experiment, baseline evaluations of each rat's electroencephalogram (EEG), mean arterial pressure (MAP), regional cerebral blood flow (r-CBF), cerebrospinal fluid (CSF) pressure, and cerebral perfusion pressure (CPP) were made. The rats were then assigned to one of three groups: Group L (n=6) received intravenous lidocaine (5 mg/kg/min); Group LE (n=6) received intravenous lidocaine (5 mg/kg/min) and epinephrine (2.5 kg/kg/min); and Group E (n=5) received intravenous epinephrine (2.5 microg/kg/min). ⋯ Neither decreased PtO2 nor extravasation of EB was observed in rats treated with epinephrine and lidocaine, excluding cerebral ischemia and BBB breakdown from possible mechanisms by which epinephrine decreased the convulsive dose of lidocaine. None of the rats in Group E exhibited EEG findings suggestive of a preconvulsive state, ruling out a convulsive effect of epinephrine itself. The results suggest that an increase in lidocaine supply to the brain caused by increased CBF causes the low cumulative dose of lidocaine at the onset of convulsion in rats given lidocaine plus epinephrine.
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J Neurosurg Anesthesiol · Jul 1998
Randomized Controlled Trial Clinical TrialTranscranial Doppler sonography mean flow velocity during infusion of ultrapurified bovine hemoglobin.
A number of studies have shown that polymerized bovine hemoglobin (HBOC-201) does not cause clinically significant side effects. This has been demonstrated in spite of the fact that a primary increase in oxygen extraction ratio has been associated with an increase in systemic vascular resistance (SVR) and a decrease in cardiac index (CI). The current study investigated the effects of HBOC-201 on cerebral circulation. ⋯ Cardiac indices were significantly lower in Group 1 (1.7-1.8 l/minute x m(-2)) than in Group 2 (2.4-2.7 l/minute x m(-2)) after PM 3. After hemodilution, mean flow velocity showed an insignificant increase in both groups, ranging from 39 to 46 cm/second. Although SVR increased significantly following HBOC-201 -infusion, the results of this study did not reveal changes in cerebral blood flow that establish significant group-to-group differences.
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J Neurosurg Anesthesiol · Jul 1998
Comparative StudyThe effects of mild hypothermia on thiopental-induced electroencephalogram burst suppression.
Thiopental intravenous injections before temporary clipping and mild hypothermia have protective effects in the setting of cerebral ischemia, and are used clinically in some centers. However, it is not known whether mild hypothermia affects thiopental-induced electroencephalogram (EEG) burst suppression. In this study, the authors compared the onset and duration of EEG suppression by thiopental in normothermic (n=10) and mildly hypothermic (n=10) patients undergoing cerebral aneurysm surgery. ⋯ Onset time was shortened (25.8+/-1.4 versus 43.5+/-5.6 seconds), and duration of suppression (531.0+/-56.6 versus 165.0+/-16.9 seconds) and the maximum duration of isoelectric EEG (47.7+/-5.8 versus 22.8+/-2.0 seconds) were prolonged in the patients with mild hypothermia. In two normothermic patients, the standard dose of thiopental did not produce burst suppression, but only a mild decrease in spectral edge frequency. The authors concluded that the effects of mild hypothermia on thiopental-induced EEG suppression are not simply additive, but synergistic.