Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Jul 1993
Randomized Controlled Trial Clinical TrialClonidine premedication for craniotomy: effects on blood pressure and thiopentone dosage.
The purpose of this study was to determine whether oral clonidine premedication improves cardiovascular stability and/or reduces the requirements for drugs used to control systolic blood pressure (SBP) during elective craniotomies. We performed a double blind randomized trial involving 77 normotensive, ASA physical status I or II adults. Clonidine 4 micrograms/kg or placebo was given as oral premedication. ⋯ Two subgroups were analyzed, based on the study groups mean age and baseline SBP. Three-way analysis of variance revealed that the blood pressure effects of clonidine were almost entirely confined to patients older than 45 years. Baseline SBP had no independent effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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J Neurosurg Anesthesiol · Jul 1993
Rate of cerebrospinal fluid formation, resistance to reabsorption of cerebrospinal fluid, brain tissue water content, and electroencephalogram during desflurane anesthesia in dogs.
Intracranial pressure (ICP) has been shown to increase dramatically during desflurane anesthesia, possibly as a result in part of an increase in the rate of cerebrospinal fluid (CSF) formation (Vf) or a decrease in the rate of CSF reabsorption. To examine this phenomenon, I designed a study to measure Vf, resistance to reabsorption of CSF (Ra), brain tissue water content, and the electroencephalographic activity (EEG) during desflurane anesthesia in dogs. Vf and Ra were determined using ventriculocisternal perfusion of mock CSF labeled with blue dextran. ⋯ The experimental conditions for groups 1 and 2 were (a) baseline (halothane 0.5-1.0% inspired plus thiopental 12 mg.kg-1 i.v. given over 15 min followed by i.v. infusion at 12 mg.kg-1 x h-1), (b) 0.5 MAC (3.5 +/- 0.1% expired) and (c) 1.0 MAC (7.0 +/- 0.1% expired) desflurane at normal CSF pressure, and (d) and (e) 0.5 and 1.0 MAC desflurane at increased CSF pressure (> 30 cm H2O). Group 3 (n = 6), the control group, was examined over the same time period as groups 1 and 2. In the control group, desflurane was not administered; instead, the baseline condition (i.e., halothane plus thiopental) was maintained throughout the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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J Neurosurg Anesthesiol · Apr 1993
Neurosurgical intensive care unit organization and function: an American experience.
This article describes the organization and function of a university-based neurosurgical intensive care unit. The unit's success has been based in part on its physical structure and in larger part on its organization. ⋯ This type of approach promotes teamwork and fosters mutual respect among the team. It also improves patient care and, frequently, outcome.
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J Neurosurg Anesthesiol · Oct 1992
End-tidal carbon dioxide as an indicator of arterial carbon dioxide in neurointensive care patients.
The relationship between the arterial partial pressure of carbon dioxide (Paco2) and the end-tidal carbon dioxide partial pressure (PEtco2) was evaluated in 11 critically ill adult neurointensive care patients during mechanical ventilation. It was hypothesized that the Paco2 to PEtco2 gradient, or P(a-Et)co2, was maintained and that PEtco2 can be used to determine Paco2 accurately in these patients. After approval by the Clinical Investigations Committee, when clinically indicated arterial blood gases (with Paco2) were measured, the PEtco2 was determined from the capnograph (Hewlett Packard 78520A infrared capnometer). ⋯ The direction of Paco2 change was inaccurately predicted by PEtco2 changes in 31.9% of measurements. PEtco2 does not provide a stable reflection of Paco2 in all neurointensive care patients. Arterial blood gases cannot be eliminated when monitoring respiratory acid-base balance in mechanically ventilated neurointensive care patients.
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J Neurosurg Anesthesiol · Jul 1992
Cerebral blood flow at constant cerebral perfusion pressure but changing arterial and intracranial pressure: relationship to autoregulation.
Therapeutic agents for reducing raised intracranial pressure (ICP) may do so at the expense of reduced mean arterial pressure (MAP). As a consequence, cerebral perfusion pressure (CPP) = (MAP - ICP) may not improve. It is unknown whether the level of MAP alters cerebral blood flow (CBF) when MAP and ICP change in parallel so that CPP remains constant. ⋯ At a CPP of 40 mm Hg, CBF showed a linear correlation with blood pressure (BP) (r = 0.57, p <0.05). These results demonstrate that when autoregulation is impaired, there is a functional difference between autoregulating and nonautoregulating cerebral vessels despite similar MAP and CPP. These results also show that at a CPP of 40 mm Hg when autoregulation is impaired, CBF depends more on arterial driving pressure than on CPP.