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Biomedical subjects

T J Ebert

Publications and source records attributed to T J Ebert.

At least 37 records · Page 2Linked to original sources
PubMed1997

Myocardial ischemia and adverse cardiac outcomes in cardiac patients undergoing noncardiac surgery with sevoflurane and isoflurane. Sevoflurane Ischemia Study Group.

UNLABELLED: Sevoflurane is associated with less tachycardia and coronary vasodilation than isoflurane and thus might be associated with less myocardial ischemia. This multicenter study examined the incidence of myocardial ischemia and adverse cardiac outcomes in adults (40-87 yr) with cardiac disease having elective noncardiac surgery. Patients were randomized to receive either sevoflurane (S) (n = 106) or isoflurane (I) (n = 108) in conjunction with sodium thiopental, vecuronium, fentanyl, and 50%-70% N2O. Intraoperative hemodynamics were maintained within 20% of awake baseline with standard drugs. A Holter monitor was applied 3-24 h before surgery and maintained until 48 h after surgery. Electrocardiograms and blood samples for analysis of the MB isoenzyme fraction of creatine phosphokinase were obtained preoperatively and daily for 48 h postoperatively. Anesthetic exposure (1.79 +/- 0.15 [mean +/- SE] minimum alveolar concentration-hour) and duration of surgery (219 +/- 13 min) did not differ between groups. The incidence of ischemia in the pre-, intra- and postoperative periods, adverse cardiac outcomes (18% occurrence), intraoperative hemodynamic variations (+/-20% change from ward baseline), and administration of adjunct cardiovascular medications were similar between groups. In cardiac patients having noncardiac surgery, sevoflurane was comparable to isoflurane with respect to the incidence of intra- and postoperative myocardial ischemia and in the frequency of adverse cardiac outcomes. IMPLICATIONS: Surgical patients with heart disease are at risk of heart complications, some of which could be induced by an anesthetic. We compared the incidence of cardiac complications between patients receiving sevoflurane and isoflurane. We found that the frequency of additional heart problems in cardiac patients receiving sevoflurane was not different from that associated with isoflurane.

Adult↗
PubMed1997

The effects of premedication on inhaled induction of anesthesia with sevoflurane.

UNLABELLED: The effects of premedication with midazolam (M), fentanyl (F), or both (B) on induction of anesthesia via a mask with sevoflurane (S) were assessed in 24 healthy volunteers who participated on three occasions, receiving either intravenous (IV) F (2.4 microg/kg), M (36 microg/kg), or B (0.6 microg/kg F, 9 microg/kg M) 5 min before three vital capacity breaths of 8% S, 66% N2O, and O2. At loss of lid-lash reflex (LLR), ventilation was manually assisted until a randomly assigned time of administration was attained, at which time laryngoscopy and tracheal intubation were attempted. The effective times for 50% of subjects (ET50) to loss of LLR were 64 s for M and B and 54 s for F (P < 0.05). The ET50 to acceptable intubating conditions were 4.3, 3.1 and 2.5 min for F, M, and B, respectively. F resulted in more airway management difficulties than M or B. Heart rate was slightly increased before intubation in M. Heart rate increases after intubation were least in F, intermediate in B, and greatest in M. The time to achieve good intubating and airway conditions up to intubation was lowest with M or B. Anesthetic adjuvants did not improve the time to achieve loss of consciousness with anesthetic induction via the face mask with sevoflurane, but they significantly decreased the time to acceptable tracheal intubating conditions. IMPLICATIONS: Adults can be anesthetized with very few side effects by breathing themselves to sleep with sevoflurane. Giving patients small doses of sedatives intravenously before they inhale an anesthetic can improve the speed and quality of the process of falling asleep.

Administration, Inhalation↗
PubMed1997

Mechanisms whereby propofol mediates peripheral vasodilation in humans. Sympathoinhibition or direct vascular relaxation?

BACKGROUND: Anesthetic induction and maintenance with propofol are associated with decreased blood pressure that is, in part, due to decreased peripheral resistance. Several possible mechanisms whereby propofol could reduce peripheral resistance include a direct action of propofol on vascular smooth muscle, an inhibition of sympathetic activity to the vasculature, or both. This study examined these two possibilities in humans by measuring the forearm vascular responses to infusions of propofol into the brachial artery (study 1) and by determining the forearm arterial and venous responses to systemic (intravenous) infusions of propofol after sympathetic denervation of the forearm by stellate blockade (study 2). METHODS: Bilateral forearm venous occlusion plethysmography was used to examine forearm vascular resistance (FVR) and forearm vein compliance (FVC). Study 1 used infusion of intralipid (time control) and propofol at rates between 83 and 664 micrograms/min into the brachial artery of 11 conscious persons and compared responses to arterial infusions of sodium nitroprusside (SNP) at 0.3, 3.0, and 10 micrograms/min. Venous blood from the infusion arm was assayed for plasma propofol concentrations. In study 2, after left stellate block (12 ml 0.25% bupivacaine + 1% lidocaine), six participants were anesthetized and maintained with propofol infusions of 125 and 200 micrograms.kg-1.min-1. Simultaneous right forearm (unblocked) blood flow dynamics served as the time control. In three additional conscious participants, intrabrachial artery infusions of SNP and nitroglycerin, both at 10 micrograms/min, were performed before and after stellate blockade of the left forearm to determine whether the sympathetically denervated forearm vessels could dilate beyond the level produced by denervation alone. RESULTS: In study 1, infusion of intralipid or propofol into the brachial artery did not change FVR or FVC. Sodium nitroprusside significantly decreased FVR in a dose-dependent manner by 22 +/- 5%, 65 +/- 3%, and 78 +/- 2% (mean +/- SEM) but did not change FVC. During the incremental propofol infusions, plasma propofol concentrations increased from 0.2 to 10.1 micrograms/ml and averaged 7.4 +/- 1.1 micrograms/ml during the highest infusion rate. In study 2, stellate ganglion blockade decreased FVR by 50 +/- 6% and increased FVC by 58 +/- 10%. Propofol anesthesia at 125 and 200 micrograms.kg-1.min-1 progressively reduced mean arterial pressure. In the arm with sympathetic denervation, FVR and FVC showed no further changes during propofol anesthesia, whereas in the control arm FVR significantly decreased by 41 +/- 9% and 42 +/- 7%, and FVC increased significantly by 89 +/- 27% and 85 +/- 32% during 125 and 200 micrograms.kg-1.min-1 infusions of propofol, respectively. In the three additional conscious participants, intraarterial infusion of SNP and nitroglycerin (TNG) after the stellate blockade resulted in a further decrease of FVR and a further increase of FVC. CONCLUSIONS: In contrast to SNP infusions, propofol infusions into the brachial artery of conscious persons caused no significant vascular responses, despite the presence of therapeutic plasma concentrations of propofol within the forearm. The effects of propofol anesthesia on FVR and FVC are similar to the effects of sympathetic denervation by stellate ganglion blockade. Thus the peripheral vascular actions of propofol appear to be due primarily to an inhibition of sympathetic vasoconstrictor nerve activity.

Adult↗
PubMed1996

Neurocirculatory responses to intubation with either an endotracheal tube or laryngeal mask airway in humans.

STUDY OBJECTIVE: To compare the sympathetic and hemodynamic responses to intubation with either an endotracheal tube (ETT) or laryngeal mask airway (LMA). DESIGN: Prospective, randomized, single-blinded study. SETTING: The in vivo study was carried out in an experimental laboratory. PATIENTS: 16 healthy male consenting volunteers, ages 20 to 31 years, were studied. INTERVENTIONS: After placement of a radial artery catheter, ECG electrodes, and a recording needle in the peroneal nerve, subjects were anesthetized with propofol 2.5 mg/kg, paralyzed with vecuronium 0.15 mg/kg, and ventilated via mask for 5 minutes with oxygen and 0.5 MAC desflurane or 0.5 MAC isoflurane. A LMA or ETT was inserted and neurocirculatory responses were continuously recorded. MEASUREMENTS AND MAIN RESULTS: Measurements of heart rate (HR), mean arterial pressure (MAP), and sympathetic nerve activity (SNA) were made at preintubation baseline and at the peak response after airway manipulation. The time to recovery to 20% and 10% of baseline MAP and HR also was measured. Neurocirculatory variables did not differ in either the LMA (n = 7) or ETT (n = 9) groups immediately prior to intubation. The ETT group demonstrated a 27% HR increase and a 42% MAP increase compared with a 12% HR increase and a 23% MAP increase in the LMA group. Muscle SNA increased 600% in the ETT group versus 66% in the LMA group (p < 0.01). The time to return MAP and HR to 20% and 10% of perintubation baseline was significantly longer in the ETT than the LMA group (p < 0.01). CONCLUSIONS: Because of the substantial reduction in the neurocirculatory responses to the LMA versus ETT, the LMA may prove advantageous in patients in whom HR and MAP increases may predispose to adverse cardiac or cerebrovascular events.

Adult↗
PubMed1996

Alfentanil modifies the neurocirculatory responses to desflurane.

Activation of the sympathetic nervous system occurs in response to desflurane, causing tachycardia and hypertension. Fentanyl partially blunts the hemodynamic effects of desflurane but fails to attenuate the sympathetic response. This study determined the clinical effectiveness and dose response of alfentanil on the neurocirculatory responses to desflurane. Twenty-five healthy, male volunteers were randomized into one of three groups to receive either placebo (n = 9), 10 micrograms/kg intravenous (IV) bolus alfentanil (n = 9), or 20 micrograms/kg IV bolus alfentanil (n = 7) in conjunction with anesthetic induction by propofol, 2.5 mg/kg. Mean arterial pressure (MAP, radial artery), heart rate (HR), and efferent muscle sympathetic nerve activity (SNA, peroneal nerve) were recorded. After conscious baseline measurements, anesthesia was induced by propofol and alfentanil/placebo. One minute later, the desflurane vaporizer was activated at 11%. Neurocirculatory measurements were recorded for 11 min. There were no differences between the groups at conscious baseline. Induction of anesthesia was associated with significantly decreased MAP in the placebo and the 10 micrograms/kg alfentanil groups and increased HR in all groups with little change in SNA. In placebo subjects, desflurane administration increased HR and MAP above baseline. In both alfentanil groups, during desflurane administration HR and MAP never increased significantly above baseline. However, SNA was significantly increased in both groups. Alfentanil effectively blunts the hemodynamic changes but not the sympathetic responses associated with rapid increases in the inspired concentration of desflurane.

Administration, Inhalation↗
PubMed1996

Desflurane-mediated neurocirculatory activation in humans. Effects of concentration and rate of change on responses.

BACKGROUND: Rapid increases in the inspired concentration of desflurane have been associated with sympathetic activation, tachycardia, hypertension, and in select cases, myocardial ischemia. The current study examined the effects of the rate of change of the desflurane concentration on the sympathetic and hemodynamic responses to desflurane and sought to determine whether a finite concentration (end-tidal) of desflurane consistently initiated these responses. METHODS: After Institutional Review Board approval, 23 healthy male volunteers were instrumented for electrocardiogram (heart rate (HR)), intraarterial blood pressure, and peroneal nerve microneurography (sympathetic nerve activity (SNA)). Subjects were given propofol (2.5 mg/kg) and vecuronium (0.15 mg/kg), and their lungs were mechanically ventilated for 30 min at a minimum alveolar concentration of 0.5 MAC with either desflurane or isoflurane (random assignment). The end-tidal concentration was increased at either 1% per min (n = 7) or 0.5% per min (n = 7) for desflurane or 0.16% per min (n = 9) for isoflurane (MAC-multiple comparable to 1% per min desflurane group) until 1.5 MAC was reached. HR, blood pressure, and SNA were averaged over 1-min segments from 0.5 to 1.5 MAC levels. RESULTS: Awake neurocirculatory variables did not differ among the three groups. At 0.5 MAC, blood pressure had decreased (12-15%) and HR increased (12-20%) similarly in both groups. SNA decreased 77% in the isoflurane group but was not significantly changed in the desflurane groups. In the desflurane groups, the threshold (end-tidal concentration associated with a 10% increase in the measured variable) ranged between 4% and 10% for HR and between 4% and 7.7% for SNA. In the isoflurane group, the threshold occurred between 1.0% and 1.6% for HR and between 0.7% and 1.3% for SNA. The rate of change did not affect the threshold concentration or the peak HR increase in the desflurane groups. In contrast, SNA responses to desflurane were directly proportional to the rate of change. CONCLUSION: There was no consistent threshold for the neurocirculatory activation associated with desflurane, and the HR and SNA thresholds generally were less than 1 MAC. The HR increase associated with desflurane was not rate- or concentration-dependent. In contrast, SNA responses were proportional to the rate of change and the concentration of desflurane.

Adult↗
PubMed1996

Induction of anesthesia and tracheal intubation with sevoflurane in adults.

BACKGROUND: The speed, quality, and cost of mask induction of anesthesia and laryngeal mask airway insertion or tracheal intubation were studied in young non-premedicated volunteers given high inspired concentrations of sevoflurane (6 to 7%). METHODS: Twenty healthy persons who were 19 to 32 years old participated three times, received 6 l/min fresh gas flow, and were randomized to receive 6 to 7% sevoflurane in 66% nitrous oxide/28% oxygen by face mask until tracheal intubation (treatment 1) or until laryngeal mask airway insertion (treatment 3), or 6 to 7% sevoflurane without nitrous oxide to tracheal intubation (treatment 2). Participants exhaled to residual volume and took three vital capacity breaths of the gas mixture; thereafter ventilation was manually assisted. The time of exposure to the inhaled gas was varied for consecutive participants. It was either increased or decreased by 30-sec increments based on the failure or success of the preceding volunteer's response to laryngoscopy and intubation after a preselected exposure time. Failure was defined as poor jaw relaxation, coughing or bucking, or inadequate vocal cord relaxation. RESULTS: Loss of the lid-lash reflex in unpremedicated young volunteers was achieved in 1 min and did not differ among groups. Average time (and 95% confidence interval) for acceptable conditions for LMA insertion was achieved in 1.7 (0.7 to 2.7) min, and all participants had an immediate return of spontaneous ventilation. The time for acceptable tracheal intubating conditions after manual hyperventilation by mask was 4.7 (3.7 to 5.7) min and 6.4 (5.1 to 7.7) min in treatments 1 and 2, respectively. There were no cases of increased secretions or laryngospasm. The incidence of breath holding and expiratory stridor ("crowing") was 7.5% and 25%, respectively, during treatment 1 and 15% and 40%, respectively, during treatment 2. CONCLUSIONS: The induction of anesthesia to loss of lid reflex in young non-premedicated adults approaches the speed of intravenous induction techniques. No untoward airway responses were noted during mask induction of anesthesia with a three-breath technique. In response to intubation, no adverse airway responses, including jaw tightness, laryngospasm, and excessive coughing or bucking, occurred in participants whose duration of mask administration of sevoflurane met the appropriate times (as determined in this study).

Adult↗
PubMed1996

Site(s) mediating sympathetic activation with desflurane.

BACKGROUND: Three strategies were employed to better define the afferent site(s) at which desflurane initiates its neurocirculatory activation. METHODS: Young (aged 19-28 yr) healthy volunteers were employed in three separate studies. Monitoring included electrocardiography, radial artery blood pressure, and direct recordings of sympathetic outflow to skeletal muscle blood vessels by microneurography. In each study, anesthesia was established with 2.5 mg/kg propofol, and in studies 1 and 2 was maintained with 5.4% desflurane via a double-lumen tube. In study 1 (n = 7) a double-lumen tube was placed with the bronchial cuff just below the vocal cords to selectively give 14.5% desflurane or 2.4% isoflurane to the upper airway (via the tracheal lumen) or lower airway (via the bronchial lumen). Study 2 (n = 14) consisted of standard placement of a left side double-lumen tube to selectively increase the inspired desflurane concentration of either right or left lung to 11% while decreasing the inspired concentration in the opposite lung to 0%, thereby maintaining constant systemic concentrations of desflurane (gas chromatography). Study 3 consisted of lidocaine or placebo airway treatment before anesthetic induction and administration of 11% inspired desflurane by mask: group A-n = 9, topical and nebulized lidocaine, glossopharyngeal and superior laryngeal nerve blocks, and transtracheal administration of lidocaine; group B-n = 7, similar treatment as group A with placebo (saline); and group C-n = 8, systemic infusions of 2% lidocaine to match plasma concentrations of lidocaine in group A. RESULTS: In study 1, significant increases in heart rate, mean arterial pressure, and sympathetic neural activity (26%, 23%, and 62%, respectively) occurred when desflurane was directed to the upper airway. These responses were approximately twofold to sixfold larger when desflurane was given to the lower airway (lungs). There were no significant increases in these variables when isoflurane was administered to the upper airways, and a significant increase in heart rate occurred only when isoflurane was delivered to the lower airways. In study 2, separate right or left lung increases in desflurane did not change the blood concentration of desflurane or sympathetic neural activity but led to significant increases in heart rate (44%) and mean arterial pressure (32%). The simultaneous administration of desflurane to both lungs increased the millimolar (mM) concentration of desflurane in the blood from 1.17 to 2.39 mM and led to increases in sympathetic neural activity (750%), heart rate (90%), and mean arterial pressure (63%). In study 3, neither regional nor systemic administration of lidocaine reduced the significant neurocirculatory activation caused by the rapid increase in the inspired concentration of desflurane by mask. CONCLUSIONS: There are sites in the upper airway (larynx and above) that respond with sympathetic activation during rapid increases in desflurane concentration independent of systemic anesthetic changes. These responses, while lesser than those seen with rapid increases to the lung, may represent direct irritation of airway mucosa. Heart rate and mean arterial pressure responses to desflurane can be initiated by selectively increasing concentrations to either right or left lung without altering systemic levels of desflurane. From this it is inferred that there are sites within the lungs, separate from systemic sites, that mediate this response. Neither systemic lidocaine nor attempted blockade of upper airway sites with cranial nerve blocks combined with topical lidocaine was effective in attenuating the neurocirculatory activation associated with desflurane.

Adolescent↗
PubMed1996

Unilateral carotid sinus stimulation and muscle sympathetic nerve activity in man.

The carotid baroreflex influences sympathetic outflow to the peripheral circulation, yet this net response is the result of information received from both right and left carotid sinuses. To assess their individual contributions on sympathetic activity, direct measurements of muscle sympathetic nerve activity (SNA) from the peroneal nerve of the right leg were made during unilateral carotid sinus stimulation. A sustained neck pressure (approximately 25 +/- 2 mm Hg) was applied to right and left carotid sinuses, as well as bilaterally, for 5 s in 10 healthy subjects using a customized neck collar device partitioned to allow for stimulation of only one side of the neck. In addition to muscle SNA, blood pressures (radial artery) and R-R interval (RRI) changes were recorded. Muscle SNA was greater for left side neck pressure with respect to burst amplitude (left = 4.07 +/- 0.67 vs right = 2.48 +/- 0.46 microV; P < 0.05), normalized burst amplitude (388 +/- 63 vs 269 +/- 37 units; P < 0.05), burst ratio (0.64 +/- 0.05 vs 0.46 +/- 0.04; P < 0.05), and a SNA index of normalized amplitude and ratio (24832 +/- 3455 vs 6566 +/- 3259 units; P < 0.05). The combined values of the muscle SNA index for right and left sides (25590 +/- 4531 units) did not differ from the bilateral value (21906 +/- 3855 units; P > 0.05). These findings suggest that afferent input from the left carotid sinus may have a greater influence on efferent muscle sympathetic outflow (as measured in the right leg) and that the bilateral response may represent the summed right and left carotid inputs.

Adult↗
PubMed1996

Cardiovascular and autonomic effects of sevoflurane.

This review focuses on the effects of the newest volatile anesthetic, sevoflurane, on the cardiovascular system. In general, the cardiovascular effects of sevoflurane are quite similar to isoflurane but quite different from desflurane. Sevoflurane is not associated with increases in heart rate in adult patients and volunteers whereas higher MAC of isoflurane and desflurane and rapid increases in the inspired concentrations of these two agents have been associated with increased heart rates in unstimulated volunteers. Increasing concentrations of sevoflurane progressively decrease blood pressure and this decrease appears similar to isoflurane and desflurane. Sevoflurane is a less potent coronary vasodilator than isoflurane in rodents and it has not been associated with coronary steal in a dog model. Sevoflurane decreases myocardial contractility similar to equi-MAC concentrations of isoflurane and desflurane and does not potentiate epinephrine-induced cardiac arrhythmias. In several multi-center studies where patients with coronary artery disease or patients at high risk for coronary artery disease were randomized to receive either sevoflurane or isoflurane for cardiac or noncardiac surgery, the incidence of myocardial ischemia and infarction did not differ between treatment groups. Thus, sevoflurane has not been associated with untoward cardiovascular changes in volunteers and patients undergoing elective surgery and may have less potent effects on the vascular smooth muscle of select circulations.

Anesthetics, Inhalation↗
PubMed1995

The effects of clonidine on desflurane-mediated sympathoexcitation in humans.

This study explored the effectiveness of oral clonidine premedication in attenuating sympathetic activation, tachycardia, and hypertension triggered by desflurane. After institutional review board approval, informed consent was obtained from 15 young, healthy male volunteers. Heart rate (HR, electrocardiogram), mean arterial pressure (MAP, radial artery catheter), and central venous pressure (CVP, jugular vein) were monitored. Recordings of sympathetic nerve activity (SNA) were obtained from the peroneal nerve via percutaneously placed tungsten needles. After baseline recordings, subjects were randomized to receive either a placebo (n = 10) or 0.3 mg of clonidine (n = 9) per os (PO). One hour later, repeat recordings were obtained. Propofol (2.5 mg/kg) and vecuronium (0.15 mg/kg) were given intravenously. Ventilation via a mask (100% O2) was used to maintain normocarbia. Two minutes after propofol administration, the desflurane vaporizer was set at 3.6% (0.5 minimum alveolar anesthetic concentration [MAC]) and increased at 1-min intervals to 7.2% and 11% (1.0 and 1.5 MAC). After 10 min, the trachea was intubated and 20 min later steady-state neurocirculatory recordings were obtained at 5.4%, during the first 5 min after advancing the vaporizer from 5.4% to 11% ("transition"), and at 11%. Resting HR, MAP, and SNA were similar between the two groups. PO clonidine reduced SNA, CVP, and MAP but did not change HR. In both groups propofol decreased SNA and MAP, and increased HR. The administration of desflurane via a mask resulted in significant increases in SNA, HR, and MAP. Clonidine reduced the HR and MAP responses by approximately 30%-40% during induction and transition periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1995

Cardiovascular responses to sevoflurane: a review.

In conclusion, sevoflurane appears to be similar to isoflurane and desflurane with a few exceptions. Sevoflurane was not associated with increases in heart rate in adult patients and volunteers, whereas higher MACs of isoflurane and desflurane and rapid increases in the inspired concentrations of these two anesthetics have been associated with tachycardia. Increasing concentrations of sevoflurane progressively decrease blood pressure in a manner similar to the other volatile anesthetics, and in unstimulated volunteers this decrease may be slightly less than with isoflurane at a higher MAC. Sevoflurane appears similar to isoflurane in its effect on regional blood flows, including the hepatic, renal, and cerebral circulation. In animals, sevoflurane appears to be a slightly less potent coronary vasodilator than isoflurane, and in a dog model, sevoflurane has not been associated with coronary flow redistribution ("steal"). Sevoflurane decreases myocardial contractility in a manner similar to equianesthetic concentrations of isoflurane and desflurane, and does not potentiate epinephrine-induced cardiac arrhythmias. Sevoflurane reduces baroreflex function in a manner similar to other volatile anesthetics. In several multicenter studies where patients with CAD or patients at high risk for CAD were randomized to receive either sevoflurane or isoflurane for cardiac or noncardiac surgery, the incidence of myocardial ischemia, infarction, and cardiac outcomes did not differ between treatment groups. Thus, sevoflurane has not been associated with untoward cardiovascular changes in volunteers and patients undergoing elective surgery compared with other volatile anesthetics, and it appears to offer a more stable heart rate profile than either isoflurane or desflurane.

Adult↗
PubMed1995

Effects of fentanyl on sympathetic activation associated with the administration of desflurane.

BACKGROUND: Activation of the sympathetic nervous system occurs when desflurane is inspired shortly after anesthetic induction and when the inspired concentration of desflurane is rapidly increased during steady-state periods of anesthesia. The purpose of this study was to determine the effectiveness and dose response of fentanyl pretreatment in attenuating the neurocirculatory responses to desflurane in healthy human volunteers. METHODS: After Institutional Research Review Board approval, three study groups were selected and, in random order, received either placebo (n = 10), a 2.5-micrograms.kg-1 intravenous bolus of fentanyl citrate followed by a continuous infusion of 1 microgram.kg-1.h-1 (n = 9), or a 5.0-micrograms.kg-1 intravenous bolus followed by an infusion of 2 micrograms.kg-1.h-1 (n = 11) before the administration of desflurane. Arterial (MAP) and central venous (CVP) pressures were measured directly, and heart rate (HR) was determined indirectly. Efferent muscle sympathetic nerve activity (SNA) was recorded from the peroneal nerve by microneurography. After neurocirculatory recordings at conscious unmedicated baseline and 12 min after fentanyl administration, anesthetic induction was carried out with 2.0 mg.kg-1 propofol and 0.2 mg.kg-1 vecuronium. Neurocirculatory measurements were repeated beginning 2 min after induction when desflurane was given via mask (semiclosed circle system, 61/min fresh gas flow, 100% O2) in three incremental 1-min steps (3.6%, 7.2%, and 11%). Intubation occurred 10 min after propofol administration. Twenty minutes after intubation, recordings were obtained during two steady-state periods during which end-tidal concentrations had achieved 5.4% (0.75 MAC) and 11% (1.5 MAC) desflurane for at least 10 min. Data also were obtained during the rapid increase in the inspired gas concentration from 5.4% to 11% ("transition"). RESULTS: Neurocirculatory variables did not differ between the three groups at conscious baseline, after fentanyl, and during steady-state periods of anesthesia. Propofol administration significantly reduced SNA and MAP. The MAP reduction was enhanced in the fentanyl-treated groups. After induction, the increases in SNA and MAP associated with the administration of desflurane by mask were not significantly reduced by fentanyl. The transition from 5.4% to 11% desflurane resulted in increases in SNA, HR, MAP, and fentanyl administration significantly attenuated the HR and MAP components. At the 11% steady-state measurement period, CVP was increased and MAP was decreased from conscious baseline, and these changes were not modified by fentanyl. CONCLUSIONS: The administration of desflurane was associated with increases in SNA, HR, MAP, and CVP. Maximum sympathetic activation and hemodynamic responses occurred 4-5 min after initiating desflurane during induction and 2-3 min after increasing the inspired concentration of desflurane during the "transition" period. Although fentanyl partially attenuated the hemodynamic component in a dose-dependent fashion during the "transition" period, it did not significantly diminish the response during induction.

Adult↗
PubMed1995

A comparison of baroreflex sensitivity during isoflurane and desflurane anesthesia in humans.

BACKGROUND: Desflurane anesthesia has been associated with heart rate (HR) and sympathetic nerve activity (SNA) responses that differ from those during isoflurane anesthesia. Whether these differences might be due to better preservation by desflurane of the baroreceptor reflex control of HR or SNA in humans was examined. METHODS: Baroreflex sensitivity was assessed in 18 volunteers anesthetized with either desflurane or isoflurane. Measurements of HR, blood pressure (BP), and efferent SNA (percutaneous recordings from the peroneal nerve) were made, and baroreflex sensitivity was evaluated at conscious baseline and during 0.5, 1.0, and 1.5 MAC anesthesia. Baroreflex responses were triggered by bolus intravenous injections of nitroprusside (100 micrograms) and phenylephrine (150 micrograms). The linear portions of the baroreflex curves relating HR to mean arterial pressure and relating SNA to diastolic pressure were determined to obtain cardiac and sympathetic baroslopes, respectively. RESULTS: Cardiac (HR) baroslopes were equally diminished at increasing MAC of both anesthetics. Sympathetic baroslopes were preserved at 0.5 MAC isoflurane but diminished at 0.5 MAC desflurane. Higher MAC produced equal depression of sympathetic baroslopes with both anesthetics. CONCLUSIONS: Increasing MAC of desflurane and isoflurane anesthesia results in similar and progressive decreases in BP but dissimilar SNA and HR responses. These differences are not explained by disparate effects of these anesthetics on the baroreceptor reflex control of SNA or HR.

Adult↗
PubMed1995

Neurocirculatory responses to sevoflurane in humans. A comparison to desflurane.

BACKGROUND: Sevoflurane and desflurane are new volatile anesthetics with low blood solubilities that confer properties of rapid anesthetic induction and emergence. Desflurane has been associated with neurocirculatory excitation after the rapid increase in inspired concentrations. The current study evaluated and compared the sympathetic and hemodynamic responses associated with the administration of sevoflurane to those associated with administration of desflurane in humans. METHODS: After Institutional Review Board approval, 21 healthy, young (19-32 yr) volunteers were randomly selected for participation. Arterial and central venous pressures were measured directly, and heart rate, forearm blood flow, and plasma norepinephrine concentrations were determined indirectly. Efferent muscle sympathetic nerve activity was recorded by microneurography. After neurocirculatory recordings at conscious baseline, measurements were repeated beginning 2 min after 2 mg/kg propofol while the anesthetic was increased incrementally by mask over a 10-min period at 1%, 2%, and 3% sevoflurane (n = 12) or 3%, 6%, and 9% desflurane (n = 9). Responses to intubation were recorded and, 20 min later, recordings were evaluated during steady-state periods of 0.41, 0.83, and 1.24 MAC. Data also were obtained after steady-state 0.83 MAC measurements when the inspired gas concentration was rapidly increased to either 3% sevoflurane or 9% desflurane ("transition" to 1.24 MAC). RESULTS: Neurocirculatory variables did not differ between the two groups at conscious baseline. During the period of administration via mask and during the "transition" period, the significant increases in sympathetic nerve activity, heart rate, mean arterial pressure, and central venous pressure associated with desflurane were not observed with sevoflurane. Ten minutes after induction, mean arterial pressure and heart rate responses to intubation did not differ between groups. With increasing anesthetic concentration, there were progressive and similar decreases in mean arterial pressure in both groups and no changes in heart rate. Central venous pressure, sympathetic nerve activity, and plasma norepinephrine increased with the greater minimum alveolar concentration multiple of desflurane but not with that of sevoflurane. CONCLUSIONS: The neurocirculatory excitation seen with rapid increases in desflurane did not occur with sevoflurane. At steady-state, increasing the concentration of sevoflurane was associated with lower sympathetic nerve activity and central venous pressure and similar mean arterial pressure and heart rate with that of desflurane.

Anesthetics↗
PubMed1994

Sympathetic activation with desflurane in humans.

Although the blood pressure lowering effects of desflurane and isoflurane were similar at equi-MAC, we noted a different pattern of response during intervals of rapidly increasing the inspired concentration of desflurane, when substantial increases in SNA, HR, and MAP occurred. Because of the lower potency of desflurane compared to isoflurane, higher concentrations of desflurane are necessary to establish an adequate surgical plane of anesthesia. Although clinically relevant concentrations of isoflurane did not trigger sympathetic activation, isoflurane triggered responses at an inspired concentration (approximately 5%) nearly equal to that of desflurane. The present research demonstrates that the initial exposure to desflurane in clinically relevant concentrations following anesthetic induction and the deepening of anesthesia with higher concentrations of desflurane can be profoundly sympatho-excitatory. Considerable caution should be taken when administering desflurane to patients who may be placed at risk by these responses.

Adult↗