Yoshimitsu Sanjo

Awakening propofol concentration with and without blood-effect site equilibration after short-term and long-term administration of propofol and fentanyl anesthesia.

Background The propofol awakening concentration can vary. However, the effect site awakening propofol concentration will be a fixed value. The purpose of this study was to determine the awakening propofol concentrations obtained from infusion Schede using abrupt discontinuation of propofol (half‐maximal effective concentration [EC sub 50]) or a descending decrease in concentration to allow blood‐effect site equilibration (EC50 eq). Methods Patients undergoing short‐term (group 1) and long‐term (group 2) elective surgery were anesthetized with computer‐assisted continuous infusion of propofol and fentanyl, with both groups receiving the same propofol (3 micro gram/ml) and fentanyl (1 ng/ml) concentrations 20–30 min before the end of surgery until the end. Then both groups were further divided into two subgroups: subgroup A abrupt discontinuation, and subgroup B descending concentrations of propofol (15‐min duration per concentration). In the A subgroups, the response to verbal command was evaluated every 30 s. In the B subgroups, the blood propofol concentrations just permitting and just preventing response to command were averaged individually. The EC50 and EC50 eq values were determined by probit analysis. Results The EC50 of group 1A was 1 micro gram/ml, which was significantly less than the 1.6 micro gram/ml of group 2A (P < 0.05). The awakening time of group 1A was 5.2 +/‐ 1.8 min, which was significantly shorter than the 9.3 +/‐ 3.5 min of group 2A (means +/‐ SD). The EC50 eq of both groups 1B and 2B was 2.2 micro gram/ml. Conclusions The EC50 eq was independent of propofol infusion length, compared with the EC50. Thus the potential for hysteresis during emergence from propofol anesthesia was confirmed.

A Small Bypass Mixing Chamber for Monitoring Metabolic Rate and Anesthetic Uptake: The Bymixer

We developed a miniature mixing chamber, the bymixer, that aids in the measurement of respiratory gas metabolism and inhalation anesthetic uptake. A small fraction of total respiratory gas flow is bypassed from the inspiratory or expiratory limb of the breathing circuit to the bymixer. We tested the relationship between total flow and bypass flow. To analyze the error and response time of the system, we compared the mixed expired carbon dioxide from the bymixer (capacity, 0.3 L, ratio of bypass flow to total flow, 1/4.5) with that from a conventional 2.0-L mixing chamber in 15 volunteers and 12 anesthetized patients during spontaneous or controlled ventilation. Bypass flow correlated well with total flow (r2 = 0.999 to 1.000) when total flow ranged from 0 to 70 L/ min and the ratio of bypass flow to total flow ranged from 1/3 to 1/20. The difference between the values of mixed expired carbon dioxide from the two mixing chambers was small, ranging from−0.03 to 0.01 vol% in both of the ventilatory modes. The relative error was within 2.3% of the carbon dioxide values obtained from the conventional chamber. We observed the error at the lowest minute volume (4 L/min). The 90% response time of the bymixer (24.8 seconds) was similar to that of the conventional chamber (19.1 seconds) at a minute volume of 7.5 L/min. For clinical use, we combined a conventional breathing circuit with two bymixers, one for mixing inspired gas and the other for mixing expired gas. We found this device accurate and easy to use.

The epidural space is deeper in elderly and obese patients in the Japanese population

Background:  Epidural anaesthesia is an efficient method of providing both regional anaesthesia and post‐operative pain relief. Detection of the epidural space is critical, but it is difficult to predict the depth of the epidural space. Published results are inconsistent. We retrospectively investigated the differences in the depth of the epidural space depending on the puncture site, approach type and physical findings of patients.

Predicted Sevoflurane Partial Pressure in the Brain with an Uptake and Distribution Model: Comparison with the Measured Value in Internal Jugular Vein Blood

Objective. In order to predict the partial pressure of volatile anesthetics in brain tissue, we developed a pharmacokinetic simulation model suitable for real time application. The accuracy of this model was examined by comparing the predicted values against measured values for blood sampled from the internal jugular vein, which was used as a measure of the partial pressure in the brain. Methods. Our model consists of six compartments: alveoli, arterial blood, a group of vessel-rich organs (VRG), muscle, fat, and venous blood. A volatile anesthetic, sevoflurane partial pressure in each compartment were calculated using the parameters of volume, blood flow, and solubility for each tissue as reported in previous studies. Simulated sevoflurane partial pressures in VRG were considered to reflect those in the brain. We studied 11 patients undergoing elective abdominal surgery or mastectomy. Sevoflurane was maintained at a concentration of 3% (by vaporizer setting) for 25 min. Sampling points were at 0 min (before sevoflurane administration) and 1, 2, 4, 9, 16, and 25 min after the start of inhalation. We measured the sevoflurane partial pressure in inspiratory gas (PIS), in end-expiratory gas (PETS), in arterial blood (PaS), and in internal jugular vein blood (PjS). These values were compared against those for the simulated brain (PBSsim). Results. The sevoflurane partial pressures increased, in order from least rapid to most rapid, as follows: PjS, PBSsim, PaS, PETS, and PIS. The differences between PjS and PBSsim were significantly smaller than those between PjS and PETS at all sampling points. PBSsim did not differ significantly from PjS at any sampling points after 4 min of inhalation, while PETS differed significantly from PjS at all sampling points. Conclusion.We conclude that our model is clinically useful for predicting sevoflurane partial pressure in the brain, assuming that PjS reflects the sevoflurane partial pressure in the brain.

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.

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 &mgr;-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.

Ergonomic Automated Anesthesia Recordkeeper using a Mobile Touch Screen with Voice Navigation

Objective. To develop an ergonomically designed computerized recordkeeping tool for anesthesiologists that allows the clinician to maintain visual contact with the patient while performing recordkeeping. Methods.To simplify the human interface software, we developed two general use software components. All purpose menu type 1 (APM1) was used for entering events using a tree structured menu. APM1 was designed to adapt to the limits of human memory, by using Millers rule of 7 to guide the input process. APM1 can be considered to be a three-dimensional table list consisting of 7 vertical and 7 horizontal choices, which has further 5 tree-structured divergences. APM1 is also completely configurable by the user. All purpose menu 2 (APM2) was used to implement the system-initiated human interface where the system will prompt the user by voice for each entry. When users touch a key on APM1 and APM2, the system was designed to respond with a voice prompt. A touch-screen was also utilized and designed to fit the anesthesia machine. The screen is equipped with a small speaker for voice response and a microphone for voice recognition. The positions of the screen are adjustable supported by a long flexible limb (85 cm). Results. After improving the design, systems were assembled for 10 operating rooms. Of the multiple features of the VOCAAR user interface, the following were well accepted by users and employed daily: touch-screen input, and voice response. The noncompulsory use rate was 87% during the initial 2 weeks, increased to 94% after 2 weeks and 100% after two months. The mean sound emission by voice response (n = 10, mean ± SD) was 8.2 ± 2.3 dB at the main anesthetist site (35 cm from the speaker mounted on the touch-screen), 2.2 ± 1.3 dB at the staff site (1.5 m from the touch-screen), which was only audible for anesthesiologist but for surgeon. Discussion. An EARK system was designed to allow the user to maintain visual contact with the patient while performing recordkeeping tasks. The combination of a mobile touch screen and voice response/recognition facilitated the design goals of the system. Although the system has enjoyed universal clinical acceptance, the voice functions remain too limited to satisfy the needs of a completely handsfree user interface. Enhancements to voice recognition technology will offer the potential for improved functionality. Additional research is also needed to better define the relationship between vigilance and visual contact with the patient.

Comparative Carbon Dioxide Output Through Injured and Noninjured Peritoneum During Laparoscopic Procedures

Tension pneumoperitoneum may force gas into a small injured vessel if the opening is kept patent by surrounding tissues. However, the amount of carbon dioxide (CO2) that penetrates through injured or noninjured peritoneum has not been systematically determined. In 25 patients undergoing elective laparoscopic ultrasonography and cholecystectomy, CO2 output (VCO2) and O2 uptake (VO2) were measured at baseline and during anesthesia, pneumoperitoneum, laparoscopic surgical procedure (Surgery), and after hemostasis of the surgical field (Postsurgery). Before anesthesia,V CO2/BSA andV O2/BSA were 97.7 ± 11.3 and 116.0 ± 10.0 mlĊmin-1Ċm-2, respectively. During anesthesia, they fell to 72.3 ± 6.0 and 89.8 ± 7.6 mlĊmin-1Ċm-2 (p < 0.05). VCO2/BSA increased to 96.0 ± 11.1 at pneumoperitoneum (p < 0.05) and increased further to 126.1 ± 11.0 mlĊmin-1Ċm-2 at Surgery. It fell to 111.7 ± 10.9 mlĊmin-1Ċm-2 Postsurgery. VO2/BSA remained unchanged during pneumoperitoneum. Minute volume increased from 2.24 ± 0.20 in anesthesia to 2.89 ± 0.25, 4.01 ± 0.32, and 3.46 ± 0.28 LĊmin-1Ċm-2 during pneumoperitoneum, Surgery, and Postsurgery, respectively, to maintain PaCO2. We conclude that the amount of CO2 absorbed following pneumoperitoneum prior to surgery is lower than that during Surgery or Postsurgery. The amount of CO2 absorbed through the surgical field was 2.3 times higher than that through the nonsurgical field, while that from the peritoneum after hemostasis of surgical field was 1.6 times higher.

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.

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.