Increasing Concentrations Of Desflurane Research Articles

Esmolol pretreatment attenuates heart rate increase and parasympathetic inhibition during rapid increases in desflurane concentration: A preliminary randomized study.

Background:Rapid increases in desflurane concentration can transiently increase the heart rate (HR). Esmolol possesses a high β1-adrenoceptor selectivity and a short duration of action. This preliminary study aimed at investigating the effects of esmolol on the HR and autonomic modulation during a desflurane-induced HR increase.Methods:American Society of Anesthesiologists physical status I female subjects, aged 20 to 50 years, who were undergoing minor breast surgery were randomly assigned to 2 groups. Rapid increases in desflurane concentration were commenced after induction of anesthesia. Each subject received either i.v. saline (control group) or esmolol 0.5 mg/kg (esmolol group) before desflurane inhalation. Using time-frequency spectral analysis of HR variability, the HR indices were studied at baseline, postinduction, posttreatment, as well as at minimal alveolar concentrations of desflurane reaching 1.0, 1.3, and 1.5. The low frequency (LF) power is influenced by both the sympathetic and parasympathetic activity, whereas the high frequency (HF) power reflects the parasympathetic activity. The LF/HF ratio is thought to reflect either sympathovagal balance or sympathetic modulation.Results:Electrocardiograms for data analysis were obtained from 8 subjects in each group. Rapid increases in desflurane concentration after induction caused a HR increase. Both the corresponding LF and HF powers were low and the LF/HF ratio remained unchanged. This indicates that the desflurane-induced HR increase may be attributed to parasympathetic inhibition and may be independent of sympathetic activation. Esmolol pretreatment effectively attenuated desflurane-induced HR increase. Moreover, subjects receiving esmolol pretreatment had increased LF and HF powers, but did not have changes in their LF/HF ratios, as compared to those without esmolol.Conclusion:Esmolol pretreatment attenuates HR increase and parasympathetic inhibition during rapid increases in desflurane concentration.

Optimal dose of remifentanil for the prevention of hemodynamic responses during induction of anesthesia with desflurane

Background: This study was designed to determine the optimal dose of remifentanil single bolus for the prevention of cardiovascular disturbance due to both a rapid increase in desflurane concentration and stimulation by intubation. Methods: One hundred three adult patients were enrolled in this pros...

Desflurane-induced hemodynamic changes in patients with diabetic cardiovascular autonomic neuropathy.

Diabetic cardiovascular autonomic neuropathy (CAN) causes perioperative cardiovascular instability. A rapid increase in the desflurane concentration induces tachycardia and hypertension (HTN). This study examined the effects of the cardiovascular response to desflurane on patients with diabetic CAN. Forty diabetes mellitus (DM) patients with CAN were divided two groups: one with HTN (DM+HTN group, n = 17) and one without HTN (DM group, n = 23). The control group (n = 20) was composed of healthy patients without DM or HTN. In each group, the concentration of desflurane inspired was increased abruptly to 12.0 vol% 2 minutes after a thiopental injection. The target was to produce an end-tidal concentration of desflurane of 10.0 vol%, which was maintained until the end of the study by adjusting the vaporizer dial setting. The heart rate (HR), mean arterial pressure (MAP), and cardiac index (CI) were measured. The HR, MAP and CI increased significantly in all three groups when compared with the baseline (P<0.05). Additionally, the HR and MAP showed did not differ among the three groups at any of sampling times. However, the CI of the DM group and the DM+HTN group differed when compared with the control group at 90 and 120 seconds after intubation (P<0.05). In diabetic patients with CAN, the hemodynamic responses to a rapid increase in desflurane concentration are similar to those in non-diabetic patients before endotracheal intubation. However, after endotracheal intubation, increments in CI are blunted in diabetic patients with CAN.

A Rapid Increase in the Inspired Concentration of Desflurane Is Not Associated with Epileptiform Encephalogram

The large inspired concentration of sevoflurane (S) during mask induction of anesthesia can induce epileptiform electroencephalogram (EEG) associated with tachycardia. Tachycardia is also seen when the concentration of desflurane (D) is abruptly increased. It is not known whether this is associated with epileptiform EEG similar to S. We studied EEG and heart rate (HR) during rapidly increased concentrations of S or D in 31 females during the postintubation period of anesthesia. Anesthesia was induced with propofol and remifentanil, and the tracheas were intubated. Patients were randomized to receive either S or D in nitrous oxide-oxygen mixture after intubation, at a small dose first. After 10 min, S or D vaporizer was advanced to the highest reading of the vaporizer (7% for S, 18% for D) for 5 min. HR and EEG were recorded. Epileptiform EEG activity was recorded in eight of 15 patients in group S and in none in group D (P < 0.05). HR increased in both groups. In group S, HR increased gradually and the highest HR value was 84 bpm at 5 min after the increase in sevoflurane concentration. In group D, HR increased to 93 bpm 2 min after the increase in desflurane concentration (no significant difference, S versus D). A rapid increase in the concentration of S frequently induces epileptiform EEG during normoventilation. Tachycardia during increasing concentrations of D is not associated with epileptiform EEG. A rapid increase in the concentration of sevoflurane induces epileptiform encephalogram (EEG) with tachycardia. A rapid increase in the concentration of desflurane also induces tachycardia but is not associated with epileptiform EEG.

Comparison of Desflurane-induced Circulatory Responses by the Rate of Increase in Inhaled Desflurane Concentration

Background: A rapid increase in desflurane concentration induces tachycardia and hypertension and increases plasma catecholamine concentration. No clinical study is available as to whether the desflurane-induced circulatory responses is blunted by the rate of increase in inhaled desflurane concentration although there were many studies about methods to blunt the circulatory responses. The current study examined to compare desflurane-induced circulatory responses by the rate of increase in inhaled desflurane concentration. Methods: Unpremedicated sixty ASA physical status 1 patients, aged 20-60 years, scheduled for elective surgery under general anesthesia were randomly allocated into one of two groups. The inspired concentration of desflurane via mask was increased to 12.0 vol% abruptly (group 1), or during 120 seconds (group 2). The target was to produce an end-tidal concentration of desflurane (ETdesf) of 10.0 vol% which was maintained until the end of the study by adjusting the vaporizer setting, when necessary. Heart rate (HR), mean arterial pressure (MAP), cardiac index (CI), systemic vascular resistance (SVR), ETdesf, end-tidal concentration of carbon dioxide, and peripheral oxygen saturation were measured at baseline and every 30 seconds for 5 minutes after inhalation of desflurane and for 2 minutes after intubation. Results: HR, blood pressure, and CI were significantly increased in two groups compared with baseline, but significant differences in maximum values were not observed between two groups. There were no significant differences between groups of the ETdesf at the maximal HR and MAP. Incidences of hypertension and tachycardia were lesser in slowly increased inhaled desflurane concentration (group 2) than abruptly increased group (group 1). Conclusions: The present study demonstrates that increasing inhaled desflurane concentration slowly for mask ventilation is partially effective in attenuating desflurane-induced circulatory responses.

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

EFFECT OF DESFLURANE AND HALOTHANE ON PHENYLEPHRINE-INDUCED CONTRACTION IN ISOLATED RAT AORTIC SMOOTH MUSCLE

Introduction. The local interaction between desflurane and sympathetic agonists remains unclear. An increase in desflurane concentration results in sympathetic activation which is not fully inhibited by blockade of airway irritation [1]. In vivo studies on chronically instrumented animals demonstrate a reduced systemic vascular resistance. Therefore, we compared the direct interaction of desflurane and halothane with phenylephrine (PE) in an isolated vascular smooth muscle preparation. A second series of experiments investigated the influence of nitric oxide (NO) inhibition on the effect of desflurane on a similar preparation. Methods. 36 300-400 gram male Wistar rats were studied. Endothelial-free 3 mm thoracic aortic rings were suspended from a force transducer in oxygenated modified Krebs-Ringer bicarbonate solution at 37[degree sign]C. A dose-response curve was constructed for each preparation using 10-7 M, 10-6 M and 10-5 M PE and repeated in the presence of both 2 MAC desflurane and halothane (n=16). A second series of experiments examined the effect of 1, 2 and 3 MAC desflurane and halothane on 10-6 M PE contractions (n=12). Finally, we examined the effect of a NO antagonist, NG-nitro-L-arginine (L-NNA) on contractions of an endothelial-intact preparation in the presence of desflurane (n=8). Statistical analysis was with the paired two-tailed student's t-test and repeated measures ANOVA. Results. Contractions were significantly greater at 10-6 and 10 (-5) M PE in the presence of 2 MAC desflurane (p<0.05) (Figure 1). ANOVA demonstrated a significant difference between the desflurane and halothane data (p=0.03). 1 and 2 MAC desflurane significantly increased contraction amplitude in response to 10 (-6) M PE (p<0.05). Halothane significantly reduced contraction amplitude at 3 MAC (p<0.05). ANOVA revealed a significant difference between the two curves (p=0.02). In the presence of L-NNA, desflurane had a greater effect (Figure 2).Figure 1Figure 2Discussion. Desflurane may cause local catecholamine release from nerve endings which may explain the interaction with phenylephrine. NO inhibition appears to increase the effect. This study may have implications for anaesthetic management of vasopressor-dependent or septic patients.

Intravenous Lidocaine Does Not Attenuate the Cardiovascular and Catecholamine Response to a Rapid Increase in Desflurane Concentration

GORMLEY, WILLIAM P.; MURRAY, JAMES M.; TRINICK, THOMAS R.; Zarmsky, Roxanne M.D. Author Information

Intravenous Lidocaine Does Not Attenuate the Cardiovascular and Catecholamine Response to a Rapid Increase in Desflurane Concentration

Intravenous Lidocaine Does Not Attenuate the Cardiovascular and Catecholamine Response to a Rapid Increase in Desflurane Concentration

Cardiovascular stimulation induced by rapid increases in desflurane concentration in humans results from activation of tracheopulmonary and systemic receptors.

It was hypothesized that stimulation of rapidly adapting airway receptors produces the transient (2-4 min) circulatory responses to rapid increases in desflurane concentrations greater than 6%. Accordingly, it was reasoned that increasing the concentration of desflurane in one lung, without altering the concentration of desflurane in systemic blood, should cause cardiovascular stimulation, whereas once the airway receptors had adapted to the stimulation, an initial increase in the systemic concentration of desflurane should have little effect. After placement of a double-lumen endotracheal tube in four volunteers and establishment of a steady-state level of 4% desflurane in both lungs, the desflurane concentration was rapidly increased from 4% to 8% in one lung while decreasing it in the other, thereby obviating any increase in the systemic desflurane blood concentration (confirmed by analysis). After returning the desflurane end-tidal concentration to 4% in both lungs, this process was repeated for the contralateral lung thereby having exposed both lungs to 8% desflurane without increasing the systemic desflurane concentration. After returning desflurane concentration to 4%, it was increased in both lungs simultaneously to 8% and consequently in blood to 8% of an atm. Rapid increases in desflurane concentrations in either lung, but not blood, significantly increased heart rate (17 +/- 5 beats/min, mean +/- SE, P < 0.05) and mean arterial blood pressure (15 +/- 5 mmHg, P < 0.05), but a greater increase in heart rate (43 +/- 5 beats/min, P < 0.05) and mean arterial blood pressure (46 +/- 11 mmHg, P < 0.05) occurred when both lungs were exposed simultaneously to rapidly increased desflurane concentration for the second time within 90 min. This result did not differ from the increase occurring on another day when both lungs and blood were exposed for the first time that day to 8% desflurane (heart rate 40 +/- 7 beats/min, P = 0.8; mean arterial blood pressure 40 +/- 3 mmHg, P = 0.5). It was concluded that at least two sites respond to a rapid increase in desflurane concentrations greater than 6%: one site in the airways and/or lungs, and at least one other in a highly perfused tissue(s). The systemic site contributes more importantly.

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)

Rapid Increase in Desflurane Concentration Is Associated with Greater Transient Cardiovascular Stimulation than with Rapid Increase in Isoflurane Concentration in Humans

Rapid Increase in Desflurane Concentration Is Associated with Greater Transient Cardiovascular Stimulation than with Rapid Increase in Isoflurane Concentration in Humans

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.