Blood Pressure, but Not Cerebrospinal Fluid Fentanyl Concentration, Predicts Duration of Labor Analgesia From Spinal Fentanyl

2010 ◽  
Vol 54 (5) ◽  
pp. 230-231
Author(s):  
&NA;
2010 ◽  
Vol 112 (1) ◽  
pp. 174-180 ◽  
Author(s):  
Kenneth E. Nelson ◽  
Timothy T. Houle ◽  
James C. Eisenach

Background There is a wide variability in dilution of drugs in cerebrospinal fluid after spinal injection, as measured near the site of injection. With local anesthetics, there is a wide variability in speed of onset, which correlates with block duration. The authors tested whether local cerebrospinal fluid drug concentrations and onset time would predict duration of analgesia from spinal fentanyl in laboring women. Methods After written informed consent, fentanyl (50 microg) was injected using the combined spinal epidural method in 56 women requesting analgesia for labor. The stylet was reinserted in the spinal needle, and 60 s later, the cerebrospinal fluid was aspirated for fentanyl assay. Time to analgesia and duration of analgesia were recorded, and data were analyzed by linear regression. Results Fifty-two women were included for data analysis. The cerebrospinal fluid fentanyl concentrations were 3.1 +/- 5.9 microg/ml, with a 7-fold range (0.9-5.9 microg/ml). Fentanyl concentration did not correlate with onset, initial sensory level at 5 and 10 min, or duration of analgesia. Decreased diastolic and increased systolic blood pressure and lower parity, but not fentanyl concentrations, correlated with longer labor analgesia. The resultant model was predictive when applied to data from four previous studies of spinal opioid analgesia duration. Conclusions Contrary to our hypothesis, the local concentration of fentanyl in the cerebrospinal fluid 1 min after injection was not correlated with onset or duration of labor analgesia. The unexpected but consistent relationship between blood pressure and combined spinal epidural analgesia duration suggests that resting hemodynamic state affects the distribution and/or clearance of intrathecally administered opioids.


2002 ◽  
Vol 96 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Rupert Kett-White ◽  
Peter J. Hutchinson ◽  
Pippa G. Al-Rawi ◽  
Marek Czosnyka ◽  
Arun K. Gupta ◽  
...  

Object. The aim of this study was to investigate potential episodes of cerebral ischemia during surgery for large and complicated aneurysms, by examining the effects of arterial temporary clipping and the impact of confounding variables such as blood pressure and cerebrospinal fluid (CSF) drainage. Methods. Brain tissue PO2, PCO2, and pH, as well as temperature and extracellular glucose, lactate, pyruvate, and glutamate were monitored in 46 patients by using multiparameter sensors and microdialysis. Baseline data showed that brain tissue PO2 decreased significantly, below a mean arterial pressure (MAP) threshold of 70 mm Hg. Further evidence of its relationship with cerebral perfusion pressure was shown by an increase in mean brain tissue PO2 after drainage of CSF from the basal cisterns (Wilcoxon test, p < 0.01). Temporary clipping was required in 31 patients, with a mean total duration of 14 minutes (range 3–52 minutes), causing brain tissue PO2 to decrease and brain tissue PCO2 to increase (Wilcoxon test, p < 0.01). In patients in whom no subsequent infarction developed in the monitored region, brain tissue PO2 fell to 11 mm Hg (95% confidence interval 8–14 mm Hg). A brain tissue PO2 level below 8 mm Hg for 30 minutes was associated with infarction in any region (p < 0.05 according to the Fisher exact test); other parameters were not predictive of infarction. Intermittent occlusions of less than 30 minutes in total had little effect on extracellular chemistry. Large glutamate increases were only seen in two patients, in both of whom brain tissue PO2 during occlusion was continuously lower than 8 mm Hg for longer than 38 minutes. Conclusions. The brain tissue PO2 decreases with hypotension, and, when it is below 8 mm Hg for longer than 30 minutes during temporary clipping, it is associated with increasing extracellular glutamate levels and cerebral infarction.


1992 ◽  
Vol 82 (6) ◽  
pp. 625-630 ◽  
Author(s):  
Kaoru YAMADA ◽  
Atsuo GOTO ◽  
Chen HUI ◽  
Noriko YAGI ◽  
Tsuneaki SUGIMOTO

1. The effects of intravenous injection of Fab fragments of anti-digoxin IgG (Digibind) on the changes in blood pressure, urine volume and urinary sodium excretion after intracerebroventricular infusion of artificial cerebrospinal fluid with normal or high sodium concentration were examined in anaesthetized rats. 2. The biological efficacy of Digibind was confirmed by experiments in vitro and in vivo, which showed that pre-treatment with Digibind completely abolished or significantly attenuated the aortic contractile response or pressor response to digoxin in guinea-pigs. 3. Infusion of high-sodium cerebrospinal fluid, but not normal-sodium cerebrospinal fluid, into the lateral brain ventricle of rats caused marked increases in blood pressure, urine volume and urinary sodium excretion. 4. Digibind did not significantly affect the increases in blood pressure, urine volume and urinary sodium excretion caused by intracerebroventricular infusion of high-sodium cerebrospinal fluid. 5. Digoxin-like immunoreactive factor may play a minor role, if any, in central nervous system-induced natriuresis in rats.


1981 ◽  
Vol 50 (5) ◽  
pp. 1011-1016 ◽  
Author(s):  
I. R. Moss ◽  
E. M. Scarpelli

Beta-Endorphin was injected into cerebrospinal fluid of lightly anesthetized dogs. Its effects on ventilation (V), tidal volume (VT), respiratory frequency (f), preinspiratory occlusion pressure (P500), and respiratory timing of unoccluded and occluded breaths were studied during CO2 rebreathing. Blood pressure and heart rate (HR) were monitored throughout the study. beta-Endorphin produced 1) early (approximately 15 min) but temporary depression of VT-PCO2 and P500-PCO2 responses; 2) progressive hypoventilation during spontaneous breathing and progressive depression of V-PCO2 and f-PCO2 responses, which were maximal at about 75 min, followed by gradual recovery; 3) progressive hypotension and bradycardia starting at about 15 min and reaching maximal effect at about 105 min. Increased expiratory time (TE) accounted for the changes in f. TE increased in unoccluded breaths and during both preinspiratory and inflation occlusion. After vagotomy, beta-endorphin produced insignificant effect on f, TE, and HR. Naloxone itself increased P500-PCO2 response; when given during beta-endorphin effect, it reversed the hypotension, bradycardia, V-PCO2, and f-PCO2 responses and facilitated the P500-PCO2 and VT-PCO2 responses. We conclude that beta-endorphin effect is produced by both depression of specific central cardiovascular and respiratory control units and facilitation of central vagal projections.


2008 ◽  
Vol 2 (1) ◽  
pp. 83-94 ◽  
Author(s):  
Rui Zou ◽  
Eun-Hyoung Park ◽  
Erin McCormack Kelly ◽  
Michael Egnor ◽  
Mark E. Wagshul ◽  
...  

Object The relationship between the waveform of intracranial pressure (ICP) and arterial blood pressure can be quantitatively characterized using a newly developed technique in systems analysis, the time-varying transfer function. This technique considers the arterial blood pressure as an input signal composed of multiple frequencies represented in the output ICP according to the transfer function imposed by the intracranial system on the input signal. The transfer function can change with time and with physiological manipulations. The authors examined data obtained from canine experiments involving manipulations of ICP. Methods The authors analyzed 11 experiments from 3 normal mongrel dogs under conditions of normal ICP and with changes in ICP made by bolus injection, infusion, or withdrawal of cerebrospinal fluid by using time-varying transfer function. Results During normal ICP periods, the gain of the transfer function displayed a deep notch (≥ 1 log unit) centered at or near the cardiac frequency. In systems terms, the intracranial compartment under normal conditions appears to act as a notch filter attenuating the cardiac frequency input relative to other frequencies. Epochs of ICP elevation showed suppression of the notch, and the notch was restored when ICP returned to normal. Conclusions The intracranial system in these animals could be considered to include a pulsation absorber for which the target frequency appears to be close to the cardiac frequency. One possible source for such an absorber mechanism might be the free movement of cerebrospinal fluid, implying that impairment of this motion may have important clinical implications in various neurological conditions such as hydrocephalus.


1911 ◽  
Vol 14 (4) ◽  
pp. 377-400 ◽  
Author(s):  
G. N. Stewart

1. The combination of a biological test object on which adrenalin causes contraction of smooth muscle (perfused blood-vessels or the uterus in certain conditions) with a biological test object on which it produces inhibition of contraction of smooth muscle (intestine) greatly diminishes the chance of error in testing blood (or other body liquids) for adrenalin. A control experiment with adrenalin solutions should, in general, accompany each observation on the blood. 2. When properly chosen biological tests are employed, no evidence is obtained of the presence of adrenalin in detectable amount in normal blood taken from the general circulation. 3. In a case of nephritis with albuminuria and persistently high arterial pressure, the pressure was diminished by forced breathing. The washing out of carbon dioxide seemed to be a factor in this diminution as well as the mechanical interference with the circulation. In this case, the administration of large doses of sodium bicarbonate was associated with a marked diminution in the blood pressure. 4. In another case with persistently high blood pressure, the drawing off of cerebrospinal fluid caused a distinct diminution in the arterial pressure, presumably by lowering the intracranial pressure. No pressor substance was detected in the cerebrospinal fluid.


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