Journal of neurosurgical anesthesiology
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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.
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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 · Apr 1998
Case ReportsA case of shock subsequent to treatment of intracranial hypertension by mannitol injection combined with hyperventilation.
This report describes a sudden decrease in blood pressure after conservative treatment of acute intracranial hypertension. A 63-year-old woman with acute hydrocephalus after undergoing clipping of an aneurysm of the right supracerebellar artery developed increased intracranial pressure, necessitating surgical management. On the operating table, the patient developed Cushing's reflex. ⋯ Fifteen minutes later, a sudden and prolonged suppression of circulation was observed (blood pressure 65/35-85/40 mmHg, heart rate 90-100 beats/min). Postoperatively, computed tomography of the head showed compression of the brain stem. We believe that this patient's blood pressure decrease was related to a sudden reduction of intracranial pressure and that mannitol injection was principally responsible for this occurrence.
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J Neurosurg Anesthesiol · Apr 1998
Clinical TrialCerebral CO2 vasoreactivity evaluation with and without changes in intrathoracic pressure in comatose patients.
It is well established that cerebral blood flow (CBF) is sensitive to variations in arterial PCO2 (PaCO2) and can be influenced by changes in jugular venous return due to elevated intrathoracic pressure. Therefore, we compared cerebral CO2 vasoreactivity when PaCO2 was altered either by changing inspired PCO2 or tidal volume. In addition, we sought to determine if noninvasive transcranial Doppler ultrasonography can be used instead of invasive CBF measurement to determine cerebral CO2 vasoreactivity. ⋯ When compared with CBF by jugular thermodilution, the rates of sensitivity and specificity of transcranial Doppler ultrasonography to detect impaired cerebral CO2 vasoreactivity were 69% and 65%, respectively. In conclusion, the reduction of PaCO2 from 40 to 25 mmHg by modifying either tidal volume or inspired PCO2 resulted in similar effects on cerebral, pulmonary, and systemic circulations. Cerebral CO2 vasoreactivity is of prognostic value in brain-injured patients when determined using CBF but may be misleading when evaluated using velocities measured by transcranial Doppler ultrasonography.
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J Neurosurg Anesthesiol · Apr 1998
The upper limit of cerebral blood flow autoregulation in acute intracranial hypertension.
The present series of experiments was performed to investigate the influence of acute intracranial hypertension on the upper limit (UL) of cerebral blood flow (CBF) autoregulation. Three groups of eight rats each--one with normal intracranial pressure (ICP) (2 mmHg), one with ICP = 30 mmHg, and one with ICP = 50 mmHg--were investigated. Intracranial hypertension was maintained by continuous infusion of lactated Ringer's solution into the cisterna magna, where the pressure was used as ICP. ⋯ At normal ICP the UL was found at a CPP of 141 +/-2 mmHg, at ICP = 30 mmHg the UL was 103+/-5 mmHg, and at ICP = 50 mmHg the UL was found at 88+/-7 mmHg. This shift of the UL was more pronounced than the shift of the lower limit (LL) of the CBF autoregulation found previously. We conclude that intracranial hypertension is followed by both a shift toward lower CPP values and a narrowing of the autoregulated interval between the LL and the UL.