Anesthetic Potency of Intravenous Infusion of 20% Emulsified Sevoflurane and Effect on the Blood-Gas Partition Coefficient in Dogs.

BACKGROUND: Intravenous (IV) infusions of volatile anesthetics in lipid emulsion may increase blood lipid concentration, potentially altering the anesthetic agent's blood solubility and blood-gas partition coefficient (BGPC). We examined the influence of a low-lipid concentration 20% sevoflurane emulsion on BGPC, and the anesthetic potency of this emulsion using dogs. METHODS: We compared BGPC and anesthetic characteristics in 6 dogs between the IV anesthesia of emulsion and the sevoflurane inhalation anesthesia in a randomized crossover substudy. Minimum alveolar concentrations (MACs) were determined by tail-clamp stimulation by using the up-and-down method. Blood sevoflurane concentration and partial pressure were measured by gas chromatography; end-tidal sevoflurane concentration was measured using a gas monitor. The primary outcome was BGPC at the end of IV anesthesia and inhalation anesthesia. Secondary outcomes were time to loss/recovery of palpebral reflex, finish intubation and awakening, MAC, blood concentration/partial pressure at MAC and awakening, correlation between blood partial pressure and gas monitor, and the safety of emulsions. RESULTS: BGPC showed no difference between IV and inhaled anesthesia (0.859 [0.850-0.887] vs 0.813 [0.791-0.901]; P = .313). Induction and emergence from anesthesia were more rapid in IV anesthesia of emulsion than inhalation anesthesia. MAC of emulsion (1.33% [1.11-1.45]) was lower than that of inhalation (2.40% [2.33-2.48]; P = .031), although there was no significant difference in blood concentration. End-tidal sevoflurane concentration could be estimated using gas monitor during IV anesthesia of emulsion. No major complications were observed. CONCLUSIONS: IV anesthesia with emulsion did not increase the BGCP significantly compared to inhalation anesthesia. It was suggested that the anesthetic potency of this emulsion may be equal to or more than that of inhalation.

A visual stethoscope to detect the position of the tracheal tube.

BACKGROUND: Advancing a tracheal tube into the bronchus produces unilateral breath sounds. We created a Visual Stethoscope that allows real-time fast Fourier transformation of the sound signal and 3-dimensional (frequency-amplitude-time) color rendering of the results on a personal computer with simultaneous processing of 2 individual sound signals. The aim of this study was to evaluate whether the Visual Stethoscope can detect bronchial intubation in comparison with auscultation. METHODS: After induction of general anesthesia, the trachea was intubated with a tracheal tube. The distance from the incisors to the carina was measured using a fiberoptic bronchoscope. While the anesthesiologist advanced the tracheal tube from the trachea to the bronchus, another anesthesiologist auscultated breath sounds to detect changes of the breath sounds and/or disappearance of bilateral breath sounds for every 1 cm that the tracheal tube was advanced. Two precordial stethoscopes placed at the left and right sides of the chest were used to record breath sounds simultaneously. Subsequently, at a later date, we randomly entered the recorded breath sounds into the Visual Stethoscope. The same anesthesiologist observed the visualized breath sounds on the personal computer screen processed by the Visual Stethoscope to examine changes of breath sounds and/or disappearance of bilateral breath sound. We compared the decision made based on auscultation with that made based on the results of the visualized breath sounds using the Visual Stethoscope. RESULTS: Thirty patients were enrolled in the study. When irregular breath sounds were auscultated, the tip of the tracheal tube was located at 0.6 +/- 1.2 cm on the bronchial side of the carina. Using the Visual Stethoscope, when there were any changes of the shape of the visualized breath sound, the tube was located at 0.4 +/- 0.8 cm on the tracheal side of the carina (P < 0.01). When unilateral breath sounds were auscultated, the tube was located at 2.6 +/- 1.2 cm on the bronchial side of the carina. The tube was also located at 2.3 +/- 1.0 cm on the bronchial side of the carina when a unilateral shape of visualized breath sounds was obtained using the Visual Stethoscope (not significant). CONCLUSIONS: During advancement of the tracheal tube, alterations of the shape of the visualized breath sounds using the Visual Stethoscope appeared before the changes of the breath sounds were detected by auscultation. Bilateral breath sounds disappeared when the tip of the tracheal tube was advanced beyond the carina in both groups.

Comparison of a new cardiac output ultrasound dilution method with thermodilution technique in adult patients under general anesthesia.

OBJECTIVE: The purpose of this study was to investigate the reliability of cardiac output (CO) measured by a new ultrasound dilution method (COud) in comparison with CO by pulmonary artery thermodilution (COtd) in adult patients undergoing surgery. DESIGN: A prospective study. SETTING: A university hospital, single institutional. PARTICIPANTS: Twenty-nine adult patients undergoing abdominal surgery. MEASUREMENTS AND MAIN RESULTS: After approval of the institutional ethics review board, 29 adult patients were evaluated. After induction, radial and pulmonary artery catheters were inserted. A disposable extracorporeal AV loop was connected between existing arterial and central venous catheters. Reusable ultrasound sensors that measure changes in blood ultrasound velocity after dilution by isotonic saline were clamped onto the arterial and venous limbs of the loop. Ultrasound dilution (UD) measurements (COstatus; Transonic Systems, Inc, Ithaca, NY) were obtained by injecting 30 mL of body-temperature isotonic saline into the venous limb of the AV loop. An average of 3 COud and 5 COtd was obtained for comparison. Bland-Altman plot and correlation analysis were used for statistical comparison. A total of 142 comparison measurements were obtained. The correlation coefficient between the 2 techniques was r = 0.91. Bland-Altman analysis did not produce any significant bias (bias = 0.02, standard deviation = 0.56). The percentage error of these data was 23.53%. CONCLUSIONS: COud measurements agreed well with COtd. The results of this study indicated that COud might be interchangeable with conventional COtd in perioperative adult patients.

The influence of hemorrhagic shock on the minimum alveolar anesthetic concentration of isoflurane in a swine model.

BACKGROUND: Although hemorrhagic shock decreases the minimum alveolar concentration (MAC) of inhaled anesthetics, it minimally alters the electroencephalographic (EEG) effect. Hemorrhagic shock also induces the release of endorphins, which are naturally occurring opioids. We tested whether the release of such opioids might explain the decrease in MAC. METHODS: Using the dew claw-clamp technique in 11 swine, we determined the isoflurane MAC before hemorrhage, after removal of 30% of the estimated blood volume (21 mL/kg of blood over 30 min), after fluid resuscitation using a volume of hydroxyethylstarch equivalent to the blood withdrawn, and after IV administration of 0.1 mg/kg of the mu-opioid antagonist naloxone. RESULTS: Hemorrhagic shock decreased the isoflurane MAC from 2.05% +/- 0.28% to 1.50% +/- 0.51% (P = 0.0007). Fluid resuscitation did not reverse MAC (1.59% +/- 0.53%), but additional administration of naloxone restored it to control levels (1.96% +/- 0.26%). The MAC values decreased depending on the severity of the shock, but the alterations in hemodynamic variables and metabolic changes accompanying fluid resuscitation or naloxone administration did not explain the changes in MAC. CONCLUSIONS: Consistent with previous reports, we found that hemorrhagic shock decreases MAC. In addition, we found that naloxone administration reversed the effect on MAC, and we propose that activation of the endogenous opioid system accounts for the decrease in MAC during hemorrhagic shock. Such an activation would not be expected to materially alter the EEG, an expectation consistent with our previous finding that hemorrhagic shock minimally alters the EEG.

Influence of hemorrhagic shock and subsequent fluid resuscitation on the electroencephalographic effect of isoflurane in a swine model.

BACKGROUND: The authors have previously reported that hemorrhage does not alter the electroencephalographic effect of isoflurane under conditions of compensated hemorrhagic shock. Here, they have investigated the influence of decompensated hemorrhagic shock and subsequent fluid resuscitation on the electroencephalographic effect of isoflurane. METHODS: Twelve swine were anesthetized through inhalation of 2% isoflurane. The inhalational concentration was then decreased to 0.5% and maintained for 25 min, before being returned to 2% and maintained for 25 min (control period). Hemorrhagic shock was then induced by removing 28 ml/kg blood over 30 min. After a 30-min stabilization period, the inhalational concentration was varied as in the control period. Finally, fluid infusion was performed over 30 min using a volume of hydroxyethyl starch equivalent to the blood withdrawn. After a 30-min stabilization period, the inhalational concentration was again varied as in the control period. End-tidal isoflurane concentrations and spectral edge frequency were recorded throughout the study. The pharmacodynamics were characterized using a sigmoidal inhibitory maximal effect model for spectral edge frequency versus effect site concentration. RESULTS: Decompensated hemorrhagic shock slightly but significantly shifted the concentration-effect relation to the left, demonstrating a 1.12-fold decrease in the effect site concentration required to achieve 50% of the maximal effect in the spectral edge frequency. Fluid resuscitation reversed the onset of isoflurane, which was delayed by hemorrhage, but did not reverse the increase in end-organ sensitivity. CONCLUSIONS: Although decompensated hemorrhagic shock altered the electroencephalographic effect of isoflurane regardless of fluid resuscitation, the change seemed to be minimal, in contrast to several intravenous anesthetics.

Influence of hypovolemia on the electroencephalographic effect of isoflurane in a swine model.

BACKGROUND: Hypovolemia alters the effect of several intravenous anesthetics by influencing pharmacokinetics and end-organ sensitivity. The authors investigated the influence of hypovolemia on the effect of an inhalation anesthetic, isoflurane, in a swine hemorrhage model. METHODS: Eleven swine were studied. After animal preparation with inhalation of 2% isoflurane anesthesia, the inhalation concentration was decreased to 0.5% and maintained at this level for 25 min before being returned to 2% (control). After 25 min, hypovolemia was induced by removing 14 ml/kg of the initial blood volume via an arterial catheter. After a 25-min stabilization period, the inhalation concentration was decreased to 0.5%, maintained at this level for 25 min, and then returned to 2% (20% bleeding). After another 25 min, a further 7 ml/kg blood was collected, and the inhalation concentration was altered as before (30% bleeding). End-tidal isoflurane concentrations and an electroencephalogram were recorded throughout the study. Spectral edge frequency was used as a measure of the isoflurane effect, and pharmacodynamics were characterized using a sigmoidal inhibitory maximal effect model for the spectral edge frequency versus end-tidal concentration. RESULTS: There was no significant difference in the effect of isoflurane among the conditions used. Hypovolemia did not shift the concentration-effect relation (the effect site concentration that produced 50% of the maximal effect was 1.2 +/- 0.2% under control conditions, 1.2 +/- 0.2% with 20% bleeding, and 1.1 +/- 0.2% with 30% bleeding). CONCLUSIONS: Hypovolemia does not alter the electroencephalographic effect of isoflurane, in contrast to several intravenous anesthetics.