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Biomedical subjects

R B Weiskopf

Publications and source records attributed to R B Weiskopf.

At least 19 recordsLinked to original sources
PubMed1995

Mathematical analysis of isovolemic hemodilution indicates that it can decrease the need for allogeneic blood transfusion.

BACKGROUND: The implementation of acute isovolemic hemodilution prior to surgical blood loss is a strategy used in an attempt to diminish the need for or obviate allogeneic transfusion and to avert the potential, attendant complications. Studies examining the efficacy of this technique have produced conflicting results. STUDY DESIGN AND METHODS: The present mathematical analysis was undertaken to resolve these conflicts by determining the efficacy of hemodilution and examining the influence of the variables affecting the outcome. Efficacy was defined as the volume of additional blood loss permitted and the volume and number of units of allogeneic blood saved from transfusion. A mathematical analysis evaluated the impact of circulating blood volume and initial and target hematocrits on the efficacy of isovolemic hemodilution. It was assumed that 1) hemodilution was completed before surgical blood loss; 2) transfusion of removed blood was begun when the target hematocrit was reached and lost surgical blood was replaced at a rate that maintained the target hematocrit; 3) allogeneic transfusion was begun after all autologous blood drawn was transfused; 4) normovolemia was maintained; and 5) a unit of allogeneic blood contains 175 mL of red cells. RESULTS: The analysis showed that isovolemic hemodilution can result in substantial additional allowable surgical blood loss that can diminish the need for or obviate allogeneic transfusion of red cells. Larger circulating blood volume, higher initial hematocrits, and lower target hematocrits increase the efficacy of hemodilution. Removal and isovolemic replacement of 1 to 2 units of blood provide minimal potential savings, as does hemodilution to a circulating (target) hematocrit of 30 percent. The extension of hemodilution to a hematocrit of (or below) 20 percent allows a disproportionately greater surgical blood loss and diminishes the need for allogeneic transfusion. It allows, for example, an additional 4.5 L of surgical blood loss, which represents a savings of 4 units of allogeneic blood when a patient with an initial blood volume of 5.0 L and a hematocrit of 45 percent undergoes isovolemic hemodilution to a hematocrit of 15 percent. CONCLUSION: Isovolemic hemodilution can diminish or in some circumstances eliminate the need for allogeneic transfusion.

Blood Transfusion↗
PubMed1995

Subanesthetic concentrations of desflurane and isoflurane suppress explicit and implicit learning.

The capacity of desflurane to suppress learning is unknown. We investigated whether a subanesthetic concentration of desflurane (0.6 minimum alevolar anesthetic concentration [MAC]) suppressed learning as much as the same concentration of isoflurane, and whether such suppression differed with increasing duration of anesthesia and intervening changes in anesthetic concentration. Using a cross-over-design study in 18-30 yr-old human volunteers, we supplied answers to Trivial Pursuit (Selchow & Righter Co., Bay Shore, NY)-like questions at 0.6 MAC desflurane and isoflurane before and after imposing a half-hour period at 1.7 MAC of each anesthetic, and behavioral directions and a category-example task at 0.6 MAC after the period at 1.7 MAC. These volunteers had a third anesthesia in which no information was supplied (control). After anesthesia, we tested whether the provision of answers during anesthesia increased the number of correct answers to Trivial Pursuit questions. We tested for the number of correct answers for information presented before versus after the 1.7-MAC period, for increased evocation of examples of categories presented during anesthesia, and for exhibition of a behavior suggested during anesthesia. We found that 0.6 MAC of both anesthetics prevented explicit and implicit learning before and after the period at 1.7 MAC.

Adolescent↗
PubMed1995

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.

Administration, Inhalation↗
PubMed1995

Implications of chemical and physical properties of desflurane for longer surgery.

Increased duration of anaesthetic administration has implications for recovery from anaesthesia, has cardiovascular effects, and potential for toxicity through metabolism and breakdown of the anaesthetics. Recovery of function after desflurane or sevoflurane anaesthesia, because of the low blood gas and tissue solubilities of these agents, is more rapid than after halothane, isoflurane or enflurane, with recovery being most rapid after desflurane. Increased duration of anaesthesia amplifies the differences in rate of recovery because of the additional anaesthetic (greater with more soluble agents) dissolved in tissues. Increased duration of anaesthesia lessens the cardiovascular depression associated with most halogenated inhaled anaesthetics including desflurane, but not isoflurane. Increased duration of anaesthesia allows for greater metabolism of anaesthetics and greater exposure to metabolites and potentially toxic breakdown products. Desflurane is the least metabolised of the available anaesthetics and is stable in soda lime and Baralyme. Thus, it has exceedingly low potential for toxicity. Sevoflurane undergoes considerable metabolism, producing free fluoride ion, with plasma concentrations proportional to dose and duration of anaesthesia exceeding 50 microM in approximately 7% of patients. In rats, the effects of a toxic breakdown product of sevoflurane, CF2 = C(CF3)OCH2F (compound A), are also dose- and duration-dependent, with lower concentrations producing toxic effects as duration of exposure increases. The clinical importance of the metabolism and in vitro breakdown of sevoflurane has still to be adequately tested.

Anesthesia Recovery Period↗
PubMed1995

Cardiovascular effects of desflurane in experimental animals and volunteers.

Desflurane (difluoromethyl-1-fluoro-2,2,2-trifluoroethyl ether [I-653]) was introduced into clinical practice in 1992. The present review summarises the current state of knowledge of the cardiovascular effects of desflurane, with emphasis on investigations published in the past 2 years, and compares desflurane's effects with those of isoflurane, and where available, sevoflurane. Desflurane produces two distinct cardiovascular actions. First, desflurane decreases left ventricular systolic and diastolic function to an extent similar to that of isoflurane. It decreases systemic vascular resistance and mean arterial blood pressure in a dose-dependent fashion. Heart rate is unchanged at lower steady-state concentrations, but increases with higher concentrations. Addition of nitrous oxide maintains heart rate unchanged, increases systemic vascular resistance and mean arterial blood pressure, but decreases cardiac output. Secondly, when the end-tidal concentration of desflurane is very rapidly increased to concentrations exceeding 1 MAC, in the absence of premedication, desflurane increases sympathetic activity, heart rate and mean arterial blood pressure. Prior administration of fentanyl, esmolol or clonidine blunts this response. The response and the ability of fentanyl to blunt it probably account for the disparate results in published studies on the use of desflurane in patients undergoing coronary artery bypass graft surgery.

Anesthetics, Inhalation↗
PubMed1994

What can we learn about the need for transfusion from patients who refuse blood? The experience with Jehovah's Witnesses.

BACKGROUND: A transfusion threshold of 7 g per dL (70 g/L) of hemoglobin has been proposed for patients, although scant human data are available to support this recommendation. STUDY DESIGN AND METHODS: The medical community's experience with Jehovah's Witnesses was examined, in order to assess the lowest tolerable hemoglobin concentration and the lower transfusion threshold of 7 g per dL (70 g/L) of hemoglobin. A MEDLINE search was conducted to capture medical and surgical reports involving Jehovah's Witnesses from 1970 through early 1993. RESULTS: Sixty-one reports of untransfused Jehovah's Witnesses with hemoglobin concentrations < or = 8 g per dL (80 g/L) or hematocrits < or = 24 percent (0.24) were identified. Of 50 reported deaths, 23, as stated in the original reports, were primarily due to anemia. Except for three patients who died after cardiac surgery, all patients whose deaths were attributed to anemia died with hemoglobin concentrations < or = 5 g per dL (50 g/L). Twenty-five survivors were reported with hemoglobin < or = 5 g per dL (50 g/L). CONCLUSION: These data have significant limitations but suggest that survival, without transfusion, is possible at low hemoglobin concentrations, while mortality with an unknown incidence is encountered at hemoglobin concentrations below 5 g per dL (50 g/L).

Anemia↗
PubMed1994

The desflurane (Tec 6) vaporizer: design, design considerations and performance evaluation.

We have described the design and design considerations of the desflurane Tec 6 "vaporizer" and have tested its performance characteristics. The vaporizer differs from previous vaporizers designed for anaesthesia in that electromechanical rather than mechanical controls accommodate the different physical characteristics of desflurane. This design, while offering perhaps an increased risk of failure (owing to sophisticated electronic components and circuitry), on the other hand offers the decreased likelihood of accidental delivery of very large concentrations of liquid anaesthetic resulting from tilting or overfilling and alarms and warnings not previously incorporated into the design of anaesthetic vaporizers. The output characteristics of the vaporizer are as expected, based on the design: desflurane concentration output in oxygen has accuracy (+/- 15%) which is similar to that of the mechanical vaporizers; output decreases when nitrous oxide is added owing to the lower viscosity, but remains within 20% of the dial setting or 0.5% absolute.

Anesthesia, Inhalation↗
PubMed1994

Humans anesthetized with sevoflurane or isoflurane have similar arrhythmic response to epinephrine.

BACKGROUND: Anesthetics can alter the dose of exogenously administered epinephrine that causes cardiac arrhythmias. The purpose of this study was to test the hypothesis that in humans anesthetized with sevoflurane, the arrhythmic response to epinephrine is not different from the response in humans anesthetized with isoflurane. METHODS: We determined the arrhythmogenicity of submucosally administered epinephrine in 40 ASA physical status 1 or 2 patients who were to undergo transsphenoidal surgery. Patients were assigned randomly to be given 1.0-1.3 minimum alveolar concentration sevoflurane or isoflurane. A surgeon, blinded to the anesthetic and the concentration of epinephrine, injected into the nasal submucosa epinephrine 10, 13.3, or 20 micrograms/ml in saline of volume sufficient for surgical need. We defined a "positive" response as three or more premature ventricular contractions within 5 min after initiation of injection. Responses between anesthetic groups within each dose range of epinephrine were compared by chi-squared analysis. RESULTS: No patient given either anesthetic developed premature ventricular contractions with doses of epinephrine less than 5 micrograms/kg. At larger doses of epinephrine (5-9.9 and 10-14.9 micrograms/kg), the frequency of arrhythmias did not differ between patients given sevoflurane and patients given isoflurane. Patients anesthetized with 1.2 minimum alveolar concentration sevoflurane had blood pressure similar to and heart rate less than those of patients anesthetized with similar concentrations of isoflurane. Blood pressure and heart rate were increased similarly in both groups after laryngoscopy and tracheal intubation and after epinephrine injection. CONCLUSIONS: Sevoflurane and isoflurane do not differ in their sensitization of the human myocardium to the arrhythmogenic effect of exogenously administered epinephrine.

Adult↗
PubMed1994

Rapid increase in desflurane concentration is associated with greater transient cardiovascular stimulation than with rapid increase in isoflurane concentration in humans.

BACKGROUND: Increases in desflurane and isoflurane concentrations can transiently increase arterial blood pressure or heart rate or both during induction of anesthesia. The current study tested the hypothesis that a rapid increase of desflurane concentration in humans increases sympathetic activity and hormonal variables and heart rate and arterial blood pressure more than does an equivalent increase in isoflurane concentration. METHODS: Twelve healthy male volunteers were assigned randomly to receive desflurane and on a separate occasion isoflurane. After induction of anesthesia with propofol 2 mg/kg, anesthesia was maintained at 0.55 MAC (desflurane, 4.0%; isoflurane 0.71% end-tidal) for 32 min. Mechanical ventilation maintained normocapnia throughout anesthesia. Mean arterial blood pressure and heart rate were recorded continuously, and arterial blood was sampled for plasma catecholamine and vasopressin (AVP) concentrations, and plasma renin activity. Anesthetic concentration was increased rapidly to 1.66 MAC (desflurane, 12.0%; isoflurane 2.12% end-tidal), and maintained at this concentration for 32 min, and then rapidly decreased to and maintained at 0.55 MAC for an additional 32 min. RESULTS: Neither anesthetic produced sympathetic or cardiovascular stimulation during their initial rapid wash-in to 0.55 MAC. The rapid increase to 1.66 MAC increased mean arterial blood pressure, heart rate, and plasma epinephrine and norepinephrine concentrations, and plasma renin activity with both desflurane and isoflurane, the former usually producing a response of greater magnitude than the latter. Plasma AVP concentration increased with desflurane only. Increased mean arterial blood pressure returned to control in 4 min. Heart rate decreased 50% of the difference between its peak and the value at 32 min at 1.66 MAC in 2 min with desflurane and in 4 min with isoflurane but did not return to the value at 0.55 MAC with either anesthetic. With desflurane, plasma epinephrine and AVP concentrations decreased quickly from their peak values, remaining elevated for 8 min. Decrease of concentrations of desflurane and isoflurane from 1.66 MAC to 0.55 MAC rapidly decreased heart rate and increased mean arterial blood pressure with both anesthetics. Thirty-two minutes after return to 0.55 MAC, with both anesthetics, only heart rate remained increased relative to the values at 32 min of the initial period of 0.55 MAC anesthesia. CONCLUSIONS: In healthy male volunteers, rapid increases of desflurane or isoflurane from 0.55 to 1.66 MAC increase sympathetic and renin-angiotensin system activity, and cause transient increases in arterial blood pressure and heart rate. Desflurane causes significantly greater increases than isoflurane, and also causes a transient increase in plasma AVP concentration. The temporal relationships suggest that the increased sympathetic activity increases mean arterial blood pressure and heart rate, with mean arterial blood pressure also increased by increased plasma AVP concentration, whereas the delayed, increased plasma renin activity is likely a response to the ensuing hypotension, or earlier inhibition by AVP, or both.

Anesthesia, General↗
PubMed1994

Rapid 1% increases of end-tidal desflurane concentration to greater than 5% transiently increase heart rate and blood pressure in humans.

BACKGROUND: Large (0.5-1.0 MAC), rapid increases of desflurane to concentrations greater than 5% can transiently increase heart rate, mean arterial blood pressure (MAP), sympathetic nerve activity, and plasma epinephrine concentration. We tested the hypothesis that small (1% = 0.14 MAC), rapid increases of desflurane concentration to greater than 5% do not increase heart rate, blood pressure, and plasma catecholamine concentrations. METHODS: Anesthesia was induced with intravenous propofol, 2 mg/kg, in 13 healthy male volunteers, 19-33 yr of age, and ventilation was controlled to maintain normocapnia. We gave 4% end-tidal desflurane in oxygen for 32 min and then imposed successive 1% increases in end-tidal desflurane concentration, each new concentration maintained for 4 min, to a final concentration of 12%. We measured heart rate, MAP and plasma catecholamine concentrations in the awake state, after 4 min at each 1% step, and at times of peak increase of MAP (> or = 10% change). RESULTS: Increases in heart rate and blood pressure of more than 10% occurred with 1% step-increases in only 1 volunteer at 5% desflurane but in 7-10 (MAP) and 8-12 (heart rate) of the 13 volunteers at higher desflurane concentrations. The 1% increases in desflurane concentration to greater than 5% also transiently increased plasma epinephrine concentrations but not vasopressin concentration or plasma renin activity in those volunteers in whom MAP increased. CONCLUSIONS: Small (1%) increases in desflurane concentration to and greater than 6% can transiently increase heart rate, mean arterial pressure, and plasma epinephrine concentration. These data and those from a previous study indicate that these increases occur with a lesser frequency and magnitude than those associated with a single, rapid step from 4% to 12% end-tidal desflurane.

Adult↗
PubMed1994

Repetitive rapid increases in desflurane concentration blunt transient cardiovascular stimulation in humans.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Adult↗
PubMed1994

Fentanyl, esmolol, and clonidine blunt the transient cardiovascular stimulation induced by desflurane in humans.

BACKGROUND: A rapid increase in the end-tidal concentration of desflurane to greater than 1 MAC transiently increases heart rate, arterial blood pressure, and circulating epinephrine and vasopressin concentrations. We hypothesized that drugs that block sympathetic activity or decrease sympathetic outflow (an opioid, a beta-adrenergic antagonist, and an alpha 2-adrenergic agonist) would blunt these responses. METHODS: After induction of anesthesia with intravenous propofol 2 mg/kg in ten healthy male volunteers age 25 +/- 1 yr (mean +/- standard error), anesthesia was maintained with 4% end-tidal desflurane in oxygen (0.55 MAC) via an endotracheal tube for 32 min. Controlled ventilation provided normocapnia. We then increased the end-tidal desflurane concentration within 1 min to 8% (1.1 MAC) and maintained this concentration for 10 min. On separate days, five of these volunteers were similarly anesthetized except that 5 min before the increase to 8% desflurane, we administered intravenous fentanyl 1.5 micrograms/kg and on another day 4.5 micrograms/kg (dose randomly assigned). On 2 separate days, intravenous esmolol 0.75 mg/kg was given to five volunteers 1.5 min before, or clonidine 4.3 micrograms/kg by mouth to four volunteers 90 min before, the increase from 4% to 8% desflurane. RESULTS: Without pretreatment, the increase to 8% desflurane increased heart rate (from 57 +/- 2 to 118 +/- 6 beats/min at peak, mean +/- standard error) and mean arterial blood pressure (from 66 +/- 2 to 118 +/- 5 mmHg). At the time of peak hemodynamic changes (within 1-2 min of the increase in desflurane concentration), plasma epinephrine and norepinephrine concentrations increased (from 22 +/- 6 to 339 +/- 83 pg/ml and from 205 +/- 19 to 283 +/- 30 pg/ml, respectively). Fentanyl 1.5 and 4.5 micrograms/kg attenuated the heart rate increase by 61 +/- 14% and 70 +/- 7% and the mean arterial blood pressure increase by 31 +/- 16% and 46 +/- 11% but did not alter the epinephrine or norepinephrine response at the time of peak cardiovascular changes. Esmolol attenuated the heart rate response but no other response. Clonidine attenuated all responses except that of norepinephrine and also caused postanesthesia sedation. CONCLUSIONS: Fentanyl, esmolol, and clonidine blunt the transient cardiovascular response to a rapid increase in desflurane concentration. Fentanyl may be the most clinically useful of these drugs because it blunts the increase in heart rate and blood pressure, has minimal cardiovascular depressant effects, and imposes little postanesthetic sedation.

Adrenergic beta-Antagonists↗
PubMed1993

Arrhythmogenic doses of epinephrine are similar during desflurane or isoflurane anesthesia in humans.

BACKGROUND: Inhaled anesthetics can alter the arrhythmogenicity of exogenously administered epinephrine. Although swine anesthetized with desflurane or isoflurane do not differ in their arrhythmic response to exogenous epinephrine, the relative effect of epinephrine in the presence of these anesthetics in humans is untested. METHODS: The authors compared the arrhythmogenicity of submucosally administered epinephrine in 36 ASA physical status 1 and 2 patients undergoing transsphenoidal resection of pituitary tumors who were randomly assigned to receive 1.0-1.3 MAC desflurane or isoflurane anesthesia. A surgeon, blinded to the administered anesthetic and the concentration of epinephrine, injected 1:50,000, 1:75,000, or 1:100,000 (20, 13.3, or 10 micrograms/ml) epinephrine in saline of volumes sufficient for surgical need. The authors defined a positive response as three or more premature ventricular contractions (PVCs) in the 5 min after starting the injection. RESULTS: No patient given either anesthetic developed any PVCs with epinephrine doses less than 7.0 micrograms/kg. Greater doses of epinephrine (7.0-13.0 micrograms/kg) produced positive responses at equal frequencies in the two anesthetic groups. CONCLUSIONS: The authors concluded that isoflurane and desflurane do not differ in their sensitization of human myocardium to the arrhythmogenic effects of exogenously administered epinephrine.

Adolescent↗
PubMed1993

Comparing the costs of inhaled anesthetics.

BACKGROUND: The immediate cost of an inhaled anesthetic results from an interplay between four factors: (1) the cost per milliliter of liquid anesthetic, (2) the volume of vapor that results from each milliliter of liquid, (3) the effective potency of the anesthetic (what concentration must be delivered from a vaporizer to provide a clinically appropriate level of anesthesia), and (4) the background flow of the gases that is chosen. A background flow that supplies only the gases/vapors required (taken up) by the patient (a "closed circuit") produces the least cost but also the least control of anesthetic level, whereas a high flow prevents rebreathing (a non-rebreathing system) but produces the greatest cost and control. We define greater "control" as a smaller ratio of delivered to alveolar concentrations. A lower solubility of an anesthetic accords the same level of control at a lower background flow rate than is achieved at a higher background flow rate with a more soluble anesthetic. Thus, a poorly soluble anesthetic may be used with a lower background flow rate than a more soluble anesthetic and may offer greater control and/or decreased cost. METHODS: This report presents a method of determining the cost of inhaled anesthetic use. As an example, the cost of delivering a desflurane anesthetic is compared with that of delivering an isoflurane anesthetic, assuming both provide an alveolar concentration of 1 MAC. The comparison is based on the pharmacokinetic differences of the two anesthetics: taking into account that for a given therapeutic anesthetic concentration (MAC), for desflurane a lower flow rate of background gas is needed to produce similar control (relationship between delivered and alveolar gases) than is needed for isoflurane. RESULTS: The analysis demonstrates that the relative cost of administering the newer and less soluble anesthetic, desflurane, can be less than, greater than, or the same as the cost of administering isoflurane, depending on the background gas inflow rate selected. CONCLUSION: The manner in which inhaled anesthetics are used and their kinetic differences are important determinants of relative cost.

Administration, Inhalation↗
PubMed1992

Desflurane does not produce hepatic or renal injury in human volunteers.

We examined the potential toxicity of desflurane in 13 young 25.0 +/- 2.3 (mean +/- SD) yr-old men, given 7.35 +/- 0.81 MAC-hours of desflurane anesthesia. Hepatic and renal function tests, serum electrolytes, and standard urine and hematologic tests were performed before, during, and after anesthesia. No toxicity was found. There were no changes in tests of hepatocellular integrity (plasma alanine transferase activity), synthetic function (serum albumin, prothrombin time, partial thromboplastin time), or renal function (serum creatinine concentration, blood urea nitrogen concentration). Decreases in red blood cell count, hematocrit, and blood hemoglobin concentration during and immediately after anesthesia were attributed to blood sampling and infusion of intravenous electrolyte solution. These values returned by 4 days after anesthesia to values not different from those before anesthesia. Increased white blood cell counts and blood glucose concentrations noted during anesthesia with other inhaled anesthetics were also seen in these volunteers. Desflurane appears to have no greater toxicity than currently used inhaled anesthetics and, because of its lesser metabolism, may have lesser or not toxicity.

Adult↗
PubMed1991

The neuromuscular effects of desflurane, alone and combined with pancuronium or succinylcholine in humans.

The neuromuscular effects of desflurane administered alone were studied in ten healthy human volunteers aged 20-27 yr. Also, the dose-response relationships of pancuronium and succinylcholine in surgical patients during anesthesia with desflurane (n = 13) were compared to those during isoflurane anesthesia (n = 14). In the volunteers, we measured the mechanical response of the adductor pollicis muscle to stimulation of the ulnar nerve in a train-of-four (TOF) sequence at 2 Hz and at tetanic frequencies of 50, 100, and 200 Hz, each administered for 5 s. Amplitudes of the first response (T1) in each TOF sequence and the ratios of the fourth TOF response (T4) to the first were similar at 3, 6, and 9% desflurane and decreased significantly only at 12% (P less than 0.05). Desflurane concentrations of 3-12% caused tetanic fade (greater than 10% decrement in amplitude) at 50, 100, and 200 Hz. The addition of N2O and the duration of anesthetic exposure did not alter desflurane's neuromuscular effects. The only neuromuscular variable influenced by CO2 was T1 amplitude, which decreased as arterial CO2 tension (PaCO2) increased. The doses of pancuronium that depressed T1 amplitude by 50% (ED50) were similar during anesthesia with 1.25 MAC desflurane, 10.5 +/- 2.8 micrograms/kg (mean +/- SD) and 1.25 MAC isoflurane, 12.3 +/- 5.0 micrograms/kg. The ED50 doses of succinylcholine were similar during anesthesia with desflurane 132 +/- 76 micrograms/kg and isoflurane 123 +/- 36 micrograms/kg. We conclude that desflurane significantly depresses neuromuscular function and augments the action of pancuronium and succinylcholine to a degree similar to that of isoflurane.

Adult↗
PubMed1991

Clinical characteristics of desflurane in surgical patients: minimum alveolar concentration.

Desflurane (formerly I-653) is a new inhalaticnal anesthetic with a promising pharmacokinetic profile that includes low solubility in blood and tissue, including fat. Since its lipid solubility is less than that of other volatile agents, it may have lower potency. Low solubility would be expected to increase the rate at which alveolar concentration approaches inspired concentration during induction as well as to increase the rate of elimination of desflurane from blood at emergence. We determined the minimum alveolar concentration (MAC) of desflurane in 44 unpremedicated ASA physical status 1 or 2 patients undergoing elective surgery. We prospectively studied four patient groups distinguished by age and anesthetic regimen: 18-30 versus 31-65 yr and desflurane in 60% N2O/40% O2 versus desflurane in O2. Anesthesia was induced with desflurane or desflurane in 60% N2O/40% O2. MAC was determined by a modification of Dixon's up-and-down method with increments of 0.5% desflurane. The MAC of desflurane in O2 was 7.25 +/- 0.0 (mean +/- SD) in the 18-30-yr age group, and 6.0 +/- 0.29 in the 31-65-yr group; the addition of 60% N2O reduced the MAC to 4.0 +/- 0.29 and 2.83 +/- 0.58, respectively. The median time from discontinuation of desflurane to an appropriate response to commands was 5.25 min. Desflurane appears to be a mild airway irritant but was well tolerated by all patients.

Adult↗