End-tidal Desflurane Research Articles

The correlation of the Narcotrend® Index and classical electroencephalographic parameters with endtidal desflurane concentrations and hemodynamic parameters in different age groups

The Narcotrend Index (NI) for assessment of depth of anesthesia by analysis of the electroencephalogram (EEG), is potentially a pharmacodynamic measure of the effects of desflurane on the brain. In this prospective study of 30 pediatric and adult patients (group 1: 3-6 years, n = 10; group 2: > 6 < 12 years; group 3: 12-40 years), undergoing ophthalmological surgery, we investigated the pharmacodynamic relationship between nonsteady state endtidal desflurane concentrations (eT(Des)), NI, classical EEG parameters (cEEG), heart rate (HR) and mean arterial pressure (MAP). The performance of the Narcotrend for differentiation between consciousness and unconsciousness was evaluated using prediction probability (P(K)). Spearman correlation analysis showed significant negative correlations (P < 0.001) between eT(Des) and NI (group 1: r = -0.93, group 2: r = -0.86, group 3: r = -0.66). Correlations between eT(Des) and MAP or HR were either only weak negative (r < -0.5) or not significant. Desflurane EC(50) (eT(Des) with half maximal effect on NI) was 7.18% for group 1, 7.34% for group 2, and 4.15% for group 3 (P < 0.001 Vs groups 1 and 2). Overall awake NI values (96.7 +/- 1.4) were significantly higher (P < 0.001) than at the moment of loss of consciousness (58.3 +/- 17.5), with no overlap (P(K) 1.0), whereas P(K) values for cEEG, MAP and HR were all <0.85. The pharmacodynamic relationship between eT(Des) and NI is age dependent with a significantly higher EC(50) in children than in adolescents and adults. The NI appears to be superior to cEEG, MAP and HR in differentiating consciousness from unconsciousness.

Effects of flow rate on hemodynamic parameters and agent consumption in low-flow desflurane anesthesia: An open-label, prospective study in 90 patients

Background: In surgical patients, decreasing the fresh gas flow rate in anesthesia may minimize costs, reduce environmental pollution, and preserve heat and humidity in the respiratory system. Objective: The aim of this study was to investigate the effects of 3 low-flowdesflurane rates on perioperative hemodynamic stability, end-tidal desflurane concentration, emergence and recovery characteristics, and agent consumption. Methods: This open-label, prospective study was conducted at the Departmentof Anesthesiology and Reanimation, University of Gaziantep, Gaziantep, Turkey. Nonpremedicated adult patients scheduled to undergo surgery (ureterolithotomy, cholecystectomy, pyelolithotomy, or thyroidectomy) were enrolled. Patients were anesthetized with propofol and fentanyl and intubated after neuromuscular blockade with vecuronium. Patients were randomly allocated to 1 of 3 groups according to the fresh gas flow rate: medium flow (2 L/min), low flow (1 L/min), and minimal flow (0.5 L/min). Intraoperative fentanyl volume was recorded. Heart rate, mean arterial pressure, and end-tidal desflurane concentration were recorded before (baseline) and after anesthesia induction; immediately before incision; and 5, 10, 15, 30, 45, and 60 minutes after incision. Emergence time and desflurane consumption after extubation were recorded. Aldrete scores were recorded at 5, 15, and 30 minutes after extubation. Results: Ninety patients (46 women, 44 men; mean [SD] age, 39.74 [13.73] years; 30 patients per treatment group) participated in the study. Means of hemodynamic parameters, intraoperative volume of fentanyl, end-tidal desflurane concentration, emergence time, and Aldrete score were statistically similar between the 3 groups. Mean (SD) desflurane consumption was significantly higher in the medium-flow group compared with the low- and minimal-flow groups (110.43 [28.18] g vs 98.40 [23.62] g and 79.80 [17.54] g, respectively; both, P < 0.01). Mean (SD) desflurane consumption was also significantly higher in the low-flow group compared with the minimal-flow group ( P < 0.01). Conclusion: The results of the present study in adult surgical patients suggestthat desflurane may be used in low-flow anesthesia, even with the minimal fresh gas flow rate.

The effects of bispectral index monitoring on end-tidal desflurane concentration

The effects of bispectral index monitoring on end-tidal desflurane concentration

Spurious bispectral index values due to electromyographic activity

EDITOR: Bispectral index monitoring (BIS) has become a standard in the monitoring of the depth of anaesthesia in many centres. Spurious BIS values may lead to inappropriate drug dosage. Too light anaesthesia may cause awareness; too deep anaesthesia may cause hypotension and delayed recovery. Several publications have reported falsely elevated BIS due to electromyographic (EMG) activity. Recently, a new electrode was developed; the BIS sensor XP Quatro® (model A2000 v.3.12; Aspect Medical Systems, Inc., Newton, MA, USA) in order to improve the signal acquisition by adding a filtering fourth plot. We report another case of a spurious BIS value with this new electrode. A 72-yr-old male was scheduled for surgery of an acoustic neuroma. Induction of anaesthesia was with propofol and remifentanil, but without any neuromuscular blocking agent, so that the facial nerve could be monitored by EMG during surgery. At induction of anaesthesia (8.05 a.m.), the BIS value decreased from 95 to 24 at 8.07 a.m. (Fig. 1) and stayed at this level until 8.18 a.m. Anaesthesia was maintained with remifentanil 0.05 μg kg−1 min−1 and desflurane 2.5% end-tidal concentration. During positioning of the head for jugular venous catheterization, the patient coughed and moved - the BIS rose to 90. The remifentanil infusion rate was progressively increased to 0.08 μg kg−1 min−1 and the end-tidal desflurane concentration to 4.7%. Twenty-two minutes later, the BIS value had not changed significantly. The quality of the signal was good as reflected by the high signal quality index. The electrode impedance was <4 kΩ at any time. Neither movement nor coughing recurred and the mean arterial pressure and heart rate decreased from 114 mmHg and 60 beats min−1, respectively, to 48 mmHg and 45 beats min−1 requiring treatment with ephedrine 12 mg (Fig. 1). We suspected an erroneous BIS value since the EMG activity was >50 at this time, despite the lack of visible forehead movement. The administration of atracurium 30 mg (8.43 a.m.) led to a decrease in EMG activity from 48 to 26 and in BIS from 82 to 30. This BIS value seemed to reflect adequately the depth of anaesthesia at this moment.Figure 1: Changes in the bispectral index, mean arterial pressure, electromyographic activity and signal quality index from the induction of anaesthesia. (······): Mean arterial pressure; bispectral index; (SYMBOL): electromyogram; signal quality index.SymbolMonitoring by BIS helps one to assess the depth of the hypnotic state and allows faster emergence and improved recovery [1]. In elderly patients, the objective is to decrease the doses of anaesthetic agents to avoid hypotension without increasing the risk of awareness. However, whatever the monitoring, there is always a risk of dysfunction or interference. False readings may lead to inappropriate decisions and serious complications. In our patient, we increased the depth of anaesthesia to a level inducing hypotension requiring the administration of ephedrine. Patient movement and coughing at jugular venous catheterization was consistent with insufficient depth of anaesthesia at this moment. The BIS then remained high despite the increase in desflurane concentration and remifentanil infusion rate. The EMG activity was measured >50 during this second period. There was clearly a parallel decrease in EMG activity and BIS after the injection of atracurium. Remifentanil has already been described as a cause of false BIS elevation by opioid-induced muscular rigidity and increased EMG activity [2]. The low-frequency muscle activity (movement) is filtered by the BIS monitor. However, muscle activity may give rise to high-frequency activity that is not filtered before signal processing. Consequently, the relative β-ratio may increase leading to BIS elevation. Other artefacts have been described due to forced air warming [3,4] or pace-maker activity [5]. In conclusion, as with other monitors, BIS readings should always be looked at critically to avoid misinterpretation leading to adverse effects, especially when the EMG activity is >45. O. Baldesi N. Bruder L. Velly F. Gouin Département d'anesthésie-réanimation; Hôpital d'adultes de la Timone; Marseilles, France

Pharmacokinetics of desflurane uptake into the brain and body

The aim of this study was to investigate the pharmacokinetics of desflurane uptake into the brain and body by comparing desflurane concentrations in internal jugular-bulb blood (Jdes), arterial blood (Ades) and pulmonary arterial blood (PAdes) at a fixed inspired desflurane concentration. Thirteen patients (aged 42-72 years) undergoing coronary artery bypass grafting surgery were enrolled in this study. They were anaesthetised using a constant 5% inspired desflurane concentration (CIdes) during the first hour of anaesthesia. Under constant volume-controlled ventilation, CIdes and end-tidal desflurane (CEdes) were measured with an infrared analyser. The desflurane concentration in the blood was analysed using gas chromatography, and cardiac output was measured using an Opti-Q pulmonary artery catheter. It took 24 min for the Jdes to equilibrate with Ades. Both CIdes-CEdes and Ades-PAdes gradients persisted during the study period. There was no further uptake of desflurane into the brain after 24 min but there was near-constant uptake into the body.

Glyburide decreases myocardial oxygen pressure in dogs.

Reports show that glyburide, an adenosine triphosphate sensitive potassium (K+ATP) channel blocker, will reverse the myocardial protective effect of inhalational anesthesia. We evaluated the effect of glyburide on myocardial tissue oxygen pressure (PmO2) in dogs anesthetized with desflurane. Twelve dogs were anesthetized with 8% end-tidal desflurane for baseline anesthesia. A flow probe was placed on the left anterior descending (LAD) artery. A probe that measured PmO2 was inserted into the middle myocardium in the LAD region. After baseline measures, six dogs received i.v. 1 mg kg(-1) of glyburide and six dogs received sham vehicle treatment. After the glyburide or sham treatment, each dog received an i.v. infusion of adenosine 0.1 microg kg(-1) x min(-1), sodium nitroprusside (SNP) 2-4 microg kg(-1) x min(-1) and 14% end-tidal desflurane in random order. Glyburide decreased LAD artery flow from 59 +/- 9 ml min(-1) to 30 +/- 6 ml min(-1) (P < 0.05) and PmO2 from 44 +/- 16 mmHg to 30 +/- 9 mmHg (P < 0.05). Adenosine infusion increased LAD artery blood flow 180% in the sham-treated dogs but produced no change in the glyburide-treated dogs. Sodium nitroprusside infusion increased LAD artery flow and decreased PmO2 in both the glyburide- and sham-treated dogs. Desflurane (14%) did not reverse the glyburide-induced vasoconstriction but increased PmO2 to 38 +/- 20 mmHg (P < 0.05). Glyburide produced myocardial tissue hypoxia, which was not changed by adenosine, worsened by SNP and improved by 14% desflurane. The improvement in PmO2 with desflurane occurred without a change in myocardial blood flow.

Electro-Acupuncture at the Zusanli, Yanglingquan, and Kunlun Points Does Not Reduce Anesthetic Requirement

We tested the hypothesis that electro-acupuncture at the Zusanli, Yanglingquan, and Kunlun acupuncture points on the legs decreases anesthetic requirement. Fourteen young, healthy volunteers were anesthetized with desflurane on two separate days. Needle electrodes were positioned at the three acupuncture points thought to produce a generalized sedative and analgesic effect. Needles were percutaneously placed on treatment days; on control days, they were insulated and taped near the insertion points. The electrodes were stimulated on the treatment day. Stimulation consisted of 2-Hz and 100-Hz currents alternated at 2-s intervals. When the end-tidal desflurane concentration of 5.5% was stable for 15 min, noxious electrical stimuli were administered via 25-gauge needles on both thighs (70 mA at 100 Hz for 10 s). Desflurane concentration was increased 0.5% when movement occurred and decreased 0.5% when it did not. An investigator, blinded to treatment, determined movement. These up-and-down sequences were continued until volunteers crossed from movement to no movement four times. A logistic regression determined the partial pressure of desflurane that produced a 50% likelihood of movement in response to noxious stimulation and consequently identified the minimum alveolar anesthetic concentration equivalent for desflurane. There was no significant difference in minimum alveolar anesthetic concentration equivalents between the electro-acupuncture (4.6% +/- 0.6%, mean +/- SD) and control (4.6% +/- 0.8%) days (P = 0.8). These data provided an 80% power for detecting a difference of 0.35 volume-percent between the groups. Electro-stimulation of three general acupuncture points on the leg did not reduce desflurane requirements. This type of acupuncture is thus unlikely to facilitate general anesthesia or decrease the need for anesthetic drugs.

Comparison of Amsorb®, Sodalime, and Baralyme®Degradation of Volatile Anesthetics and Formation of Carbon Monoxide and Compound A in Swine In Vivo

Consequences of volatile anesthetic degradation by carbon dioxide absorbents that contain strong base include formation of compound A from sevoflurane, formation of carbon monoxide (CO) and CO toxicity from desflurane, enflurane and isoflurane, delayed inhalation induction, and increased anesthetic costs. Amsorb (Armstrong Ltd., Coleraine, Northern Ireland) is a new absorbent that does not contain strong base and does not form CO or compound A in vitro. This investigation compared Amsorb, Baralyme (Chemetron Medical Division, Allied Healthcare Products, St. Louis, MO), and sodalime effects on CO (from desflurane and isoflurane) and compound A formation, carboxyhemoglobin (COHb) concentrations, and anesthetic degradation in a clinically relevant porcine in vivo model. Pigs were anesthetized with desflurane, isoflurane, or sevoflurane, using fresh or partially dehydrated Amsorb, Baralyme, and new and old formulations of sodalime. Anesthetic concentrations in the fresh (preabsorber), inspired (postabsorber), and end-tidal gas were measured, as were inspired CO and compound A concentrations and blood oxyhemoglobin and COHb concentrations. For desflurane and isoflurane, the order of inspired CO and COHb formation was dehydrated Baralyme >> soda-lime > Amsorb. For desflurane and Baralyme, peak CO was 9,700 +/- 5,100 parts per million (ppm), and the increase in COHb was 37 +/- 14%. CO and COHb increases were undetectable with Amsorb. Oxyhemoglobin desaturation occurred with desflurane and Baralyme but not Amsorb or sodalime. The gap between inspired and end-tidal desflurane and isoflurane did not differ between the various dehydrated absorbents. Neither fresh nor dehydrated Amsorb caused compound A formation from sevoflurane. In contrast, Baralyme and sodalime caused 20-40 ppm compound A. The gap between inspired and end-tidal sevoflurane did not differ between fresh absorbents, but was Amsorb < sodalime < Baralyme with dehydrated absorbents. Amsorb caused minimal if any CO formation, minimal compound A formation regardless of absorbent hydration, and the least amount of sevoflurane degradation. An absorbent like Amsorb, which does not contain strong base or cause anesthetic degradation and formation of toxic products, may have benefit with respect to patient safety, inhalation induction, and anesthetic consumption (cost).

Low-flow anaesthesia with desflurane: kinetics during clinical procedures

Background and objective Low-flow anaesthesia is economical and less polluting. The purpose of this study was to determine the inspired and end-tidal desflurane concentrations during anaesthesia with a vaporizer setting maintained at 5%, during low-flow anaesthesia after 120 min with fresh gas inflows of 1.0 and 2.0 L min−1. Methods The study was both prospective and randomized, including 56 patients (28 patients in each group) scheduled for elective surgery of an expected anaesthesia time of at least 120 min. Inspired and end-tidal concentrations of desflurane were measured during low-flow anaesthesia with fresh gas inflows of 1.0 and 2.0 L min−1. The vaporizer setting was fixed at 5% desflurane. Results The inspired and end-tidal concentrations of desflurane in the 1.0 L min−1 group after 120 min were 4.54% vs. 4.37% (P < 0.001). In the 2.0 L min−1 group, the inspired and end-tidal concentrations of desflurane were 4.76% vs. 4.58% (P < 0.001). The estimated end-tidal/inspired ratios at 120 min of anaesthesia were 0.96 in both groups. At a fresh gas flow of 1.0 L min−1, the end-tidal concentration was 0.87 of the vaporizer setting. Increasing the fresh gas flow to 2.0 L min−1 increased the end-tidal value by 0.05. Conclusion There is a significant difference between the inspired and end-tidal concentrations of desflurane when fresh gas inflows were 1.0 and 2.0 L min−1, but not for the ratio of inspired/end-tidal.

Effect of Surgical Stimuli on Desflurane-induced Electroencephalographic Changes.

Effect of Surgical Stimuli on Desflurane-induced Electroencephalographic Changes.Röpcke et al.(page 390)Röpcke et al. recruited 24 female patients scheduled to undergo abdominal surgery to investigate the effect of surgical stimuli on the concentration–response relation of desflurane-induced electroencephalographic changes. Oral midazolam, 7.5 mg, was administered to all patients 2 h before surgery, and anesthesia was induced with 2 mg/kg propofol. A 45-min waiting period was allowed for dissipation of the effects of the induction dose of propofol; during this time, 1.0 MAC desflurane was administered to the patients. The team used 12 patients as controls to determine the desflurane–electroencephalographic effect relation without noxious stimulation. With the desflurane concentration administered during the waiting period serving as a starting point, half the patients were assigned randomly to administration of a decreased desflurane concentration initially, whereas the other half were assigned to administration of an increased amount. Desflurane was increased or decreased in incremental steps, and concentrations did not exceed 1.6 MAC to avoid a high percentage of burst suppressions. Data were collected for at least 30 min.In the other 12 patients, desflurane vaporizer settings were increased or decreased after opening of the peritoneum. Decreasing the desflurane vaporizer settings was terminated if an end-tidal desflurane concentration of 0.5 MAC was achieved or if the attending anesthesiologist deemed the depth of anesthesia inadequate. Raw signals from electroencephalographic monitors were filtered and digitized. The median power frequency (the frequency below which 50% of the power lies) and spectral edge frequency 95 (the frequency below which 95% of the power lies) were calculated for each epoch. The Bispectral Index was computed from the bilateral frontal channels on a second electroencephalographic monitor. Desflurane effect-site concentrations and the concentration–effect curves for spectral edge frequency 95, median power frequency, and Bispectral Index were determined by simultaneous pharmacokinetic and pharmacodynamic modeling.The researchers found that surgical stimulation caused a shift in desflurane concentration–electroencephalographic effect curves for spectral edge frequency 95, median power frequency, and Bispectral Index toward higher desflurane concentrations. In the unstimulated group of patients, 2.2 ± 0.74 vol% desflurane was necessary to achieve a Bispectral Index of 50, whereas in the group monitored during surgery, 6.8 ± 0.98 vol% was required. Although all study participants underwent the same type of procedure (gynecologic laparotomy), the researchers concede that the level of noxious stimulation might not have remained constant throughout the data collection period. However, their results showed that surgical stimulation affects the cortical electrical activity measured by univariate electroencephalographic parameters.

-The effect of desflurane on cerebral blood flow velocity and cerebrovascular reactivity to CO2 in children-.

To assess in children with a transcranial Doppler the effect on cerebral blood flow velocities of desflurane, whose cerebral vasodilator effects have been studied in animals and in adults with intracranial lesions. Prospective clinical study. Ten healthy children, mean age: 3.4 yr, ASA physical class 1, undergoing minor urologic surgery, were included in this study. Induction was obtained with atropine 10 micrograms.kg-1, fentanyl 3 micrograms.kg-1 and propofol 3 mg.kg-1. Endotracheal intubation was facilitated by atracurium 0.3 mg.kg-1. Mechanical ventilation, with a 50% air/oxygen mixture was adjusted to achieve an end-tidal CO2 (PETCO2) level of 38 +/- 2 mmHg. Monitoring included measurement of mean arterial blood pressure (MAP), heart rate, PETCO2, SpO2 and end-tidal desflurane concentrations (FETDes). Mean blood flow velocities (Vmean) were measured in the middle cerebral artery using a bi-directional 2 MHz TCD system (EME-TC 2000 S). A first TCD measurement followed intubation (T1). Thereafter, desflurane was adjusted to 1 MAC. Six other TCDs were recorded each minute until FETDes reached the inspired fraction (T2-T7). Thereafter, CO2 reactivity was assessed with a hypocapnia test, induced by hyperventilation. Measures were done at T8 (PETCO2: 33 +/- 1 mmHg), T9 (PETCO2: 29 +/- 1 mmHg), and T10 (initial PETCO2: 38 +/- 1 mmHg). All these measurements were made before starting surgery. Analysis of variance (ANOVA) was used to analyse the data (P < 0.05 was considered as significant). The Vmean and heart rate increased significantly with increasing concentrations of desflurane (Vmean from 68 +/- 27 to 106 +/- 30 cm.s-1 and heart rate from 109 +/- 17 to 136 +/- 15 b.min-1 between T1 and T7). During hypocapnia, Vmean decreased to 68 +/- 23 cm.s-1 at T9, and returned to normal values with PETCO2 at 38 mmHg at T10. SpO2 remained unchanged. Mean arterial pressure was stable from T1 to T7, but decreased significantly at T9 and T10. Desflurane elicits a dose-dependent increase in cerebral blood flow velocities and heart rate, but does not change mean arterial pressure, suggesting that its cerebrovascular action is independent of its systemic vascular action. CO2 reactivity is maintained at one MAC. The results in children are similar to those seen in adults.

COMPARISON OF ETOMIDATE AND DESFLURANE FOR BRAIN PROTECTION DURING PROLONGED CEREBRAL ISCHEMIA

S347 Background: Previous studies indicate that etomidate produces cerebral vasoconstriction and may limit brain tissue oxygenation while desflurane increases cerebral blood flow and brain tissue oxygen availability. We compared the effects of etomidate and desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2) and pH in patients who had middle cerebral artery (MCA) occlusion for > 15 minutes and related this to patient outcome. Methods: Following a craniotomy, a probe which measures PO2, PCO2 and pH was inserted into cortex tissue at risk for ischemia during brain artery occlusion. Cerebrovascular surgery required MCA occlusion for extra-cerebral to intra-cerebral (EC-IC) bypass (n = 11) or clipping of a giant aneurysm (n = 1). A burst suppression pattern of the electroencephalogram (EEG) was induced with etomidate (n = 6) or 9% end-tidal desflurane (n = 6) before MCA occlusion. Mean blood pressure was supported with phenylephrine to 90-95 mmHg. Glascow outcome scores were evaluated before surgery and upon discharge from the Neuro Intensive Care Unit. Results: Under baseline conditions, tissue PO2, PCO2, and pH were statistically similar between the two groups. During administration of etomidate, tissue PO2 decreased in 5 of 6 patients without a change in PCO2 or pH. MCA occlusion for an average of 33 min produced tissue hypoxia (PO2 < 10 mmHg) and acidosis (pH < 7.0) in > 50% of etomidate treated patients and this was related to a poor neurological outcome. During administration of 9% desflurane, tissue PO2 and pH increased before MCA clipping. MCA occlusion for an average of 37 min produced tissue hypoxia in 2 of 6 patients without acidosis but no patient showed a worse outcome. Conclusion: These results suggest that tissue hypoxia and acidosis during MCA occlusion are indicators of ischemic injury. Treatment with desflurane may attenuate ischemic injury by improving tissue oxygenation and CO2 clearance.

Anesthetic potency of desflurane in the horse: determination of the minimum alveolar concentration.

To determine the minimum alveolar concentration (MAC) of desflurane (DES) in the horse. Prospective study. Six healthy adult horses (three males and three females) weighing 370 +/- 16 kg and aged 9 +/- 2 years old. Anesthesia was induced with DES vaporized in oxygen via a face mask connected to a large-animal, semiclosed anesthetic circle system. The horses were endotracheally intubated and positioned in right lateral recumbency. Inspired and end-tidal DES were monitored using a calibrated Ohmeda RGM 5250 multigas analyzer (Ohmeda-BOC, Spain). The MAC of desflurane that prevented gross purposeful movement in response to 60 seconds of noxious electrical stimulation of oral mucous membranes was determined. The time from the start of DES administration to lateral recumbency was 6.1 +/- 0.9 min. The MAC of DES in these horses was 7.6 +/- 0.4%. Time required for the animal to regain sternal recumbency after 98 +/- 4 minutes of anesthesia was 6.6 +/- 0.5 minutes and the time to standing was 14.3 +/- 2.7 minutes. The MAC of desflurane in these horses was 7.6 +/- 0.4%. DES provided a rapid induction to, and recovery from, anesthesia. Desflurane offers the potential for more precise control during anesthesia, and may allow a faster and uneventful recovery. It is important to know the MAC of an inhalant to use it clinically.

Sympathetic nervous system does not mediate reflex pupillary dilation during desflurane anesthesia.

Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system. Noxious stimulation dilates the pupil in both unanesthetized and anesthetized humans. In the absence of anesthesia, dilation is primarily mediated by the sympathetic nervous system. In contrast, pupillary dilation in cats given barbiturate or cloralose anesthesia is mediated solely by inhibition of the midbrain parasympathetic nucleus. The mechanism by which noxious stimuli dilate pupils during anesthesia in humans remains unknown. Accordingly, the authors tested the hypothesis that the pupillary dilation in response to noxious stimulation during desflurane anesthesia is primarily a parasympathetic reflex. In six volunteers, the alpha-I adrenergic receptors of the iris musculature were blocked by unilateral administration of topical dapiprazole; six other volunteers were given unilateral topical tropicamide to block the muscarinic receptors in the iris. Desflurane anesthesia was subsequently induced in all volunteers. Sympathetic nervous system activation, with reflex dilation of the pupil, was produced by noxious electrical stimulation during 4% and 8% end-tidal desflurane, and by a rapid 4%-to-8% step-up in the desflurane concentration. Pupil diameter and the change in pupil size induced by a light stimulus (light reflex amplitude) were measured with infrared pupillometry. Dapiprazole drops produced a Horner's miosis, but pupils were equally small after induction of anesthesia. Pupillary dilation after noxious stimulation and desflurane step-up was identical in the unblocked and dapiprazole-blocked pupils. After tropicamide administration, the pupil was dilated and the light reflex was completely inhibited. Noxious stimulation nonetheless produced a slight additional dilation. During desflurane anesthesia, pupillary dilation in response to noxious stimulation or desflurane step-up is not mediated by the sympathetic nervous system (as it is in unanesthetized persons). Although inhibition of the pupillo-constrictor nucleus may be the cause of this dilation, the mechanism remains unknown.

Cardiopulmonary effects of desflurane in ponies, after induction of anaesthesia with xylazine and ketamine.

Cardiopulmonary parameters were measured in 12 ponies (small horses) before anaesthesia and, following induction with xylazine and ketamine, during maintenance of anaesthesia with desflurane. In six of the ponies (group A) anaesthesia was maintained for three hours with desflurane at an end-tidal concentration of 7.4 per cent. In the other six ponies (group B), anaesthesia was maintained in the same way for one hour and then the effects of end-tidal desflurane concentrations of 7.4 per cent and 9.6 per cent with and without artificial ventilation were investigated. In group A ponies the arterial blood pressure and the systemic vascular resistance index (SVRI) decreased significantly during the first 45 minutes of anaesthesia but recovered with time. The cardiac index and heart rates were unchanged throughout the measurement period but arterial carbon dioxide tensions increased significantly. In group B ponies, with either mode of ventilation, increasing desflurane concentration resulted in decreases in arterial blood pressure, cardiac index and mixed venous oxygen tension, although the changes were not always statistically significant. There were marked individual differences in the cardiovascular responses to the high desflurane concentrations, the minimum mean arterial blood pressure ranging from 35 to 62 mm Hg, and the cardiac index from 23 to 50 ml/kg/min. The study concludes that during maintenance of anaesthesia with end tidal concentrations of desflurane of 7.4 per cent, cardiac index is well maintained and the initial fall in arterial blood pressures results from a fall in SVRI. However, increasing the concentration of desflurane causes a fall in blood pressure due to cardiac depression.

Cardiopulmonary effects of desflurane in the dog during spontaneous and artificial ventilation

The cardiopulomary effects of desflurane at end tidal concentrations of 103, 12·9 and 15·5 per cent during either spontaneous or artificial ventilation were studied in five beagle dogs. Desflurane anaesthesia resulted in tachycardia and a decrease in arterial blood pressure which were not significantly related to the end tidal desflurane concentrations or the mode of ventilation. At an end tidal desflurane concentration of 15·5 per cent there was a significant increase in central venous and pulmonary arterial wedge pressures and, with artificial ventilation, a reduction in cardiac output and stroke volume when compared with similar measurements at an end tidal desflurane concentration of 103 per cent. When allowed to breathe spontaneously, the dogs panted at times when they were lightly anaesthetised, but their respiration was depressed to a varying extent at the highest end tidal desflurane concentration. The induction of anaesthesia with desflurane was smooth, and the quality of anaesthesia during maintenance was excellent. There was one episode of a transient tachyarrhythmia associated with the measurement of cardiac output, but no other side effects were observed.

Suppression of spinal and cortical somatosensory evoked potentials by desflurane anesthesia.

The effect of the volatile anesthetic desflurane on spinal and cortical somatosensory evoked potentials (SEPs) was examined in 11 Sprague-Dawley male rats. Platinum recording electrodes were placed stereotactically over the left somatosensory cortex and dorsal midline of the T11-12 spinal cord while the right posterior tibial nerve was stimulated at twice motor threshold. The effect of desflurane was examined at various concentrations ranging from 0.7 to 11.4% (2 MAC). Mean arterial blood pressure (MAP) decreased (p = 0.001) progressively with increasing end-tidal desflurane concentrations. Concentrations of 1.4% (1/4 MAC) and 2.8% (1/2 MAC) did not significantly affect the spinal SEP (SSEP) amplitude or the latency. With higher concentrations, there was a progressive decrease in amplitude of the cortical SEPs (CSEPs; p = 0.002) and SSEPs (p = 0.008). However, CSEP and SSEP latencies did not change. At 5.7% (1 MAC), three animals (33%) lost CSEPs while SSEPs remained intact. At 11.4% (2 MAC), the CSEPs were lost in all animals. Only one rat lost the SSEPs at the 2 MAC concentration of desflurane, indicating the resistance of the SSEPs to desflurane anesthesia. We conclude that desflurane anesthesia significantly alters the amplitude of SSEPs and CSEPs without a significant change in the peak latency.

Fentanyl, clonidine, and repeated increases in desflurane concentration, but not nitrous oxide or esmolol, block the transient mydriasis caused by rapid increases in desflurane concentration.

Initial, but not subsequent, inhalation of 8% desflurane produces transient sympathetic stimulation. We hypothesized that initial but not subsequent increases should produce pupil dilation, and that N2O, fentanyl, and clonidine, but not esmolol, should blunt the response. In 10 volunteers, we maintained anesthesia with 4% end-tidal desflurane in oxygen for 32 min, then increased the concentration to 8% for 10 min. In nine of the volunteers, we twice repeated the increase to 8%, separating each increase by a 32-min period at 4%. On separate days, five volunteers received 4%-8% desflurane in 60% N2O; five received fentanyl 1.5 micrograms/kg or 4.5 micrograms/kg intravenously 5 min before 4%-8% desflurane; four received clonidine 4.3 micrograms/kg, orally, 90 min before 4% to 8%; and four received esmolol 0.75 mg/kg, intravenously, 1.5 min before 4%-8%. Without other drugs present, 4%-8% desflurane transiently increased pupil diameter to 5.4 +/- 0.5 mm (mean +/- SD), with subsequent 4%-8% increases producing attenuated responses (2.9 +/- 1.5 and 3.2 +/- 1.8 mm). N2O produced a higher peak (6.2 +/- 0.7 mm). Fentanyl 1.5 micrograms/kg and 4.5 micrograms/kg decreased peak diameter (2.3 +/- 0.9 and 1.6 +/- 0.3 mm), as did clonidine (2.3 +/- 1.7 mm) but not esmolol. We conclude that, concurrent with sympathetic stimulation, an initial rapid increase in desflurane concentration transiently increases pupil diameter, whereas repeated increases produce attenuated responses. N2O augments, fentanyl and clonidine attenuate, and esmolol does not affect the response.

Fentanyl, Clonidine, and Repeated Increases in Desflurane Concentration, but Not Nitrous Oxide or Esmolol, Block the Transient Mydriasis Caused by Rapid Increases in Desflurane Concentration

Initial, but not subsequent, inhalation of 8% desflurane produces transient sympathetic stimulation.We hypothesized that initial but not subsequent increases should produce pupil dilation, and that N2 O, fentanyl, and clonidine, but not esmolol, should blunt the response. In 10 volunteers, we maintained anesthesia with 4% end-tidal desflurane in oxygen for 32 min, then increased the concentration to 8% for 10 min. In nine of the volunteers, we twice repeated the increase to 8%, separating each increase by a 32-min period at 4%. On separate days, five volunteers received 4%-8% desflurane in 60% N2 O; five received fentanyl 1.5 micro gram/kg or 4.5 micro gram/kg intravenously 5 min before 4%-8% desflurane; four received clonidine 4.3 micro gram/kg, orally, 90 min before 4% to 8%; and four received esmolol 0.75 mg/kg, intravenously, 1.5 min before 4%-8%. Without other drugs present, 4%-8% desflurane transiently increased pupil diameter to 5.4 +/- 0.5 mm (mean +/- SD), with subsequent 4%-8% increases producing attenuated responses (2.9 +/- 1.5 and 3.2 +/- 1.8 mm). N2 O produced a higher peak (6.2 +/- 0.7 mm). Fentanyl 1.5 micro gram/kg and 4.5 micro gram/kg decreased peak diameter (2.3 +/- 0.9 and 1.6 +/- 0.3 mm), as did clonidine (2.3 +/- 1.7 mm) but not esmolol. We conclude that, concurrent with sympathetic stimulation, an initial rapid increase in desflurane concentration transiently increases pupil diameter, whereas repeated increases produce attenuated responses. N2 O augments, fentanyl and clonidine attenuate, and esmolol does not affect the response. (Anesth Analg 1995;81:372-8)

Repetitive Rapid increases in Desflurane Concentration Blunt Transient Cardiovascular Stimulation in Humans

Rapid increases in desflurane concentrations above minimum alveolar concentration (MAC) can cause transient (2-4-min) circulatory changes, possibly from stimulation of rapidly-adapting airway receptors. We hypothesized that the initial increase in concentration would produce greater changes than subsequent increases. Anesthesia was induced with propofol in nine volunteers (25 +/- 1 yr old, mean +/- SE) and maintained with 4% end-tidal desflurane for 32 min. We increased the desflurane to 8% (1.1 MAC) in 1 min, maintained this concentration for 10 min, and then decreased it to 4% for 32 min. We repeated this process twice. After 1 week, 5 subjects were treated similarly except that the second increase in concentration occurred 10 min and (on a separate occasion) 75 min after the initial increase. Four subjects received the initial increase after 75 rather than 32 min of anesthesia. In four we applied the repeated sequences in a background of 60% nitrous oxide. When a minimal cardiovascular response followed an increase of anesthetic concentration, a 60-s supramaximal 100-Hz tetanic stimulus was applied to an ulnar nerve percutaneously to test for sympathetic responsiveness. The initial increase in concentration increased heart rate (HR) from 57 +/- 2 to a peak of 119 +/- 7 beats/min (P < 0.05); mean arterial blood pressure (MAP) from 66 +/- 3 to 119 +/- 5 mmHg (P < 0.05); and plasma epinephrine by > 10-fold (P < 0.05). The second and third increases in desflurane concentration increased HR and MAP by less than 20% of the initial increases, regardless of the timing of the later concentration increases. Responses to initial concentration increases after 75 min of anesthesia did not differ from those after 32 min. Increases in plasma epinephrine with the second and third increases in desflurane concentration were attenuated. Subjects who did not responded to the second or third increase in desflurane always responded to tetanic electrical stimulation with substantial increases in HR and MAP (P < 0.05). Addition of nitrous oxide did not change results except for a smaller increase in MAP (P < 0.05). Ulnar nerve stimulation increased HR and MAP but not epinephrine or norepinephrine concentrations. An initial rapid increase in desflurane to 1.1 MAC produces much more stimulation than do subsequent increases, regardless of the presence of nitrous oxide. The decreased response is consistent with the hypothesis that stimulation of rapidly-adapting airway receptors produce the initial response.