Anesthesia and analgesia
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Anesthesia and analgesia · Mar 1999
Pretreatment with dexmedetomidine: altered indices of anesthetic depth for halothane in the neuraxis of cats.
The sedative and anesthetic-sparing ability of the alpha2-adrenergic agonist dexmedetomidine is well documented. In this study, we identified the effects of halothane, with and without dexmedetomidine, on hemodynamic and electroencephalographic (EEG) variables and quantified the concentration of halothane resulting in various anesthetic depth indices mediated through the central nervous system (CNS) in chronically instrumented cats. Halothane was given alone or after dexmedetomidine (15 microg/kg p.o.). In both groups, four indices of anesthetic depth--minimum alveolar anesthetic concentration (MAC; no movement to noxious stimuli), MAC(BAR) (no autonomic response to noxious stimuli), MAC(BS) (EEG burst suppression), and MAC(ISOELECTRIC) (EEG isoelectricity)--were determined. Halothane decreased arterial blood pressure, heart rate, and higher frequency components of the EEG before the onset of burst suppression and isoelectricity. Dexmedetomidine pretreatment augmented the actions of halothane on arterial pressure, heart rate, and the EEG. Dexmedetomidine reduced the halothane concentrations resulting in MAC (from 1.22% +/- 0.06% to 0.89% +/- 0.08%) and MAC(BAR) (from 1.81% +/- 0.05% to 1.1% +/- 0.10%), but not those resulting in MAC(BS) (3.01% +/- 0.17% vs 3.14% +/- 0.10%) or MAC(ISOELECTRIC) (4.39% +/- 0.26% vs 4.65% +/- 0.12%). These results suggest that dexmedetomidine does not alter various CNS-mediated indices of anesthetic action to equivalent degrees and that there are dissimilar degrees of an anesthetic-sparing action at different levels of the neuraxis. ⋯ The anesthetic adjuvant dexmedetomidine seems to differentially alter central nervous system-mediated indices of anesthetic action. Lower brainstem or spinal determinants of anesthetic depth (movement and hemodynamic responses) are more attenuated than those of higher brain functions, such as the electroencephalogram.
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Anesthesia and analgesia · Mar 1999
Comparative StudyThe incidence of fetal heart rate changes after intrathecal fentanyl labor analgesia.
We performed a retrospective review to compare the incidence of new fetal heart rate abnormalities after institution of either intrathecal fentanyl or conventional epidural labor analgesia. In chronological order, the first 100 parturients in active labor who had received epidural analgesia and had recorded fetal heart rate (FHR) traces for 30 min before and after injection were identified, as were the first 100 parturients who had received intrathecal fentanyl analgesia. A perinatologist blinded to the anesthetic technique evaluated each recording and identified any changes in the FHR between the before and after tracings. The incidence of new "negative" (implying worsened fetal status) changes was 6% in the epidural group and 12% in the intrathecal group (P > 0.05, not significant). There were no differences in incidence or degree of blood pressure change, need for cesarean delivery, neonatal outcome, parity, or oxytocin use. No parturient required urgent or emergent cesarean delivery, and all changes resolved within the 30-min observation period. A much larger study would be required to determine whether this six percentage point difference represents a true difference between groups, and its clinical significance. ⋯ We compared the incidence of fetal heart rate changes after two techniques of labor analgesia. Both techniques were associated with a low (6%-12%) incidence of changes, but a much larger series would be required to determine whether this represents a true difference. No difference in neonatal outcome was found.
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Anesthesia and analgesia · Mar 1999
Clinical TrialThe effects of in vitro hemodilution with gelatin, hydroxyethyl starch, and lactated Ringer's solution on markers of coagulation: an analysis using SONOCLOT.
Blood-saving strategies have recently been established to avoid allogeneic transfusion during surgery or after trauma. This includes an expanding use of crystalloids and colloids. These solutions interfere with coagulation systems, but quantitative measurements are still lacking. The SONOCLOT (Sienco Company, Morrison, CO) analysis (SCT), a viscoelastic test, measures clot formation and includes information on the cellular, as well as the plasmatic coagulation, system. To quantify hemodilutional effects on in vitro coagulation, we studied gelatin (G), hydroxyethyl starch 6% (HES; molecular weight 450,000), and lactated Ringer's solution (RL) in 33% and 66% dilutions measuring routines laboratory and SCT variables. Hemodilution with RL tended to increase in vitro coagulability. Among the tested colloids, G had the least impact on markers of coagulation. G33% did not differ significantly from the undiluted control group. HES had the largest impact on markers of coagulation compared with G and RL. In conclusion, SCT provides a fast and easy to perform bedside test to quantify in vitro hemodilution. ⋯ The effects of progressive hemodilution on coagulation are difficult to measure. SONOCLOT analyses provide an easy to perform test with fast information on cellular and plasmatic coagulation properties. Among colloids, hydroxyethyl starch has the largest impact on markers of coagulation compared with gelatin or lactated Ringer's solution.
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Anesthesia and analgesia · Mar 1999
Comparative StudyMeasuring brain tissue oxygenation compared with jugular venous oxygen saturation for monitoring cerebral oxygenation after traumatic brain injury.
Jugular bulb oximetry is the most widely used method of monitoring cerebral oxygenation. More recently, measurement of brain tissue oxygenation has been reported in head-injured patients. We compared the changes in brain tissue oxygen partial pressure (PbO2) with changes in jugular venous oxygen saturation (SjVO2) in response to hyperventilation in areas of brain with and without focal pathology. Thirteen patients with severe head injuries were studied. A multiparameter sensor was inserted into areas of brain with focal pathology in five patients and outside areas of focal pathology in eight patients. A fiberoptic catheter was inserted into the right jugular bulb. Patients were hyperventilated in a stepwise manner from a PaCO2 of approximately 35 mm Hg to a PaCO2 of 22 mm Hg. There was no significant change in cerebral perfusion pressure or arterial partial pressure of oxygen with hyperventilation. In areas without focal pathology, there was a good correlation between changes in SjVO2 and PbO2 (deltaSjVO2 and deltaPbO2; r2 = 0.69, P < 0.0001). In areas with focal pathology, there was no correlation between deltaSjVO, and APbO2 (r2 =0.07, P = 0.23). In this study, we demonstrated that measurement of local tissue oxygenation can highlight focal differences in regional cerebral oxygenation that are disguised when measuring SjVO2. Thus, monitoring of PbO2 is a useful addition to multimodal monitoring of patients with traumatic head injury. ⋯ Brain oxygenation is currently monitored by using jugular bulb oximetry, which attracts a number of potential artifacts and may not reflect regional changes in oxygenation. We compared this method with measurement of brain tissue oxygenation using a multiparameter sensor inserted into brain tissue. The brain tissue monitor seemed to reflect regional brain oxygenation better than jugular bulb oximetry.
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Anesthesia and analgesia · Mar 1999
Clinical TrialThe nature of spontaneous recovery from mivacurium-induced neuromuscular block.
The hypothesis of this study was that, in a given patient, recovery from a tracheal intubating dose of mivacurium would indicate the time course of spontaneous recovery after discontinuation of an infusion of mivacurium. Thirty-eight male patients consented to participate in the study. After induction of anesthesia and endotracheal intubation, the ulnar nerve was stimulated with train-of-four (TOF) stimuli at 12-s intervals. Patients received 0.3 mg/kg mivacurium in two evenly divided doses of 0.15 mg/kg each, separated by 30 s. Complete ablation of TOF responses occurred in most patients. Once the first twitch in the TOF (T ) had recovered to 25% of its baseline height, a mivacurium infusion was begun to maintain 95% suppression of T1. As surgery was nearing completion, the infusion was discontinued, and neuromuscular function was allowed to recover spontaneously. Data were analyzed for recovery intervals after the administration of the initial doses of mivacurium and after discontinuation of the infusion. Analysis of variance was used to determine the strength of correlation between the time from administration of the initial 0.3 mg/kg dose to 5% recovery of T1 and the times to recovery of TOF ratios of 70% and 90%. The 25%-75% recovery interval after discontinuation of the infusion ranged from 2.8 to 11.3 min. The time interval after administration of mivacurium 0.3 mg/kg to 5% recovery of T1 correlated with both the time to recovery of a TOF ratio of 70% and 90%. Recovery to a TOF of 90% after discontinuation of the infusion required approximately the same amount of time as recovery to 5% T1 after the administration of 0.3 mg/kg mivacurium. Each patient's recovery of neuromuscular function after discontinuation of a mivacurium infusion was related to his recovery after the administration of 0.3 mg/kg mivacurium. Therefore, the need for pharmacologic antagonism of block can be anticipated well before the end of an anesthetic. ⋯ Mivacurium (0.3 mg/kg) was administered to 38 patients. As they began to recover muscle strength, a mivacurium infusion was begun and later discontinued as surgery was nearing completion. Each patient's early recovery (administration to 5% recovery of T1) after the initial dose of mivacurium correlated well with more complete recovery of muscle strength after discontinuation of an infusion. This relationship enables early prediction of recovery speed after a mivacurium infusion.