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Biomedical subjects

D I Sessler

Publications and source records attributed to D I Sessler.

At least 73 records · Page 4Linked to original sources
PubMed2000

Efficacy of two methods for reducing postbypass afterdrop.

BACKGROUND: Afterdrop, defined as the precipitous reduction in core temperature after cardiopulmonary bypass, results from redistribution of body heat to inadequately warmed peripheral tissues. The authors tested two methods of ameliorating afterdrop: (1) forced-air warming of peripheral tissues and (2) nitroprusside-induced vasodilation. METHODS: Patients were cooled during cardiopulmonary bypass to approximately 32 degrees C and subsequently rewarmed to a nasopharyngeal temperature near 37 degrees C and a rectal temperature near 36 degrees C. Patients in the forced-air protocol (n = 20) were assigned randomly to forced-air warming or passive insulation on the legs. Active heating started with rewarming while undergoing bypass and was continued for the remainder of surgery. Patients in the nitroprusside protocol (n = 30) were assigned randomly to either a control group or sodium nitroprusside administration. Pump flow during rewarming was maintained at 2.5 l x m(-2) x min(-1) in the control patients and at 3.0 l x m(-2) x min(-1) in those assigned to sodium nitroprusside. Sodium nitroprusside was titrated to maintain a mean arterial pressure near 60 mm Hg. In all cases, a nasopharyngeal probe evaluated core (trunk and head) temperature and heat content. Peripheral compartment (arm and leg) temperature and heat content were estimated using fourth-order regressions and integration over volume from 18 intramuscular needle thermocouples, nine skin temperatures, and "deep" hand and foot temperature. RESULTS: In patients warmed with forced air, peripheral tissue temperature was higher at the end of warming and remained higher until the end of surgery. The core temperature afterdrop was reduced from 1.2+/-0.2 degrees C to 0.5+/-0.2 degrees C by forced-air warming. The duration of afterdrop also was reduced, from 50+/-11 to 27+/-14 min. In the nitroprusside group, a rectal temperature of 36 degrees C was reached after 30+/-7 min of rewarming. This was only slightly faster than the 40+/-13 min necessary in the control group. The afterdrop was 0.8+/-0.3 degrees C with nitroprusside and lasted 34+/-10 min which was similar to the 1.1+/-0.3 degrees C afterdrop that lasted 44+/-13 min in the control group. CONCLUSIONS: Cutaneous warming reduced the core temperature afterdrop by 60%. However, heat-balance data indicate that this reduction resulted primarily because forced-air heating prevented the typical decrease in body heat content after discontinuation of bypass, rather than by reducing redistribution. Nitroprusside administration slightly increased peripheral tissue temperature and heat content at the end of rewarming. However, the core-to-peripheral temperature gradient was low in both groups. Consequently, there was little redistribution in either case.

Adult↗
PubMed2000

Perioperative heat balance.

Hypothermia during general anesthesia develops with a characteristic three-phase pattern. The initial rapid reduction in core temperature after induction of anesthesia results from an internal redistribution of body heat. Redistribution results because anesthetics inhibit the tonic vasoconstriction that normally maintains a large core-to-peripheral temperature gradient. Core temperature then decreases linearly at a rate determined by the difference between heat loss and production. However, when surgical patients become sufficiently hypothermic, they again trigger thermoregulatory vasoconstriction, which restricts core-to-peripheral flow of heat. Constraint of metabolic heat, in turn, maintains a core temperature plateau (despite continued systemic heat loss) and eventually reestablishes the normal core-to-peripheral temperature gradient. Together, these mechanisms indicate that alterations in the distribution of body heat contribute more to changes in core temperature than to systemic heat imbalance in most patients. Just as with general anesthesia, redistribution of body heat is the major initial cause of hypothermia in patients administered spinal or epidural anesthesia. However, redistribution during neuraxial anesthesia is typically restricted to the legs. Consequently, redistribution decreases core temperature about half as much during major conduction anesthesia. As during general anesthesia, core temperature subsequently decreases linearly at a rate determined by the inequality between heat loss and production. The major difference, however, is that the linear hypothermia phase is not discontinued by reemergence of thermoregulatory vasoconstriction because constriction in the legs is blocked peripherally. As a result, in patients undergoing large operations with neuraxial anesthesia, there is the potential of development of serious hypothermia. Hypothermic cardiopulmonary bypass is associated with enormous changes in body heat content. Furthermore, rapid cooling and rewarming produces large core-to-peripheral, longitudinal, and radial tissue temperature gradients. Inadequate rewarming of peripheral tissues typically produces a considerable core-to-peripheral gradient at the end of bypass. Subsequently, redistribution of heat from the core to the cooler arms and legs produces an afterdrop. Afterdrop magnitude can be reduced by prolonging rewarming, pharmacologic vasodilation, or peripheral warming. Postoperative return to normothermia occurs when brain anesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. However, residual anesthesia and opioids given for treatment of postoperative pain decreases the effectiveness of these responses. Consequently, return to normothermia often needs 2-5 h, depending on the degree of hypothermia and the age of the patient.

Body Temperature Regulation↗
PubMed2000

Smoking decreases alveolar macrophage function during anesthesia and surgery.

BACKGROUND: Smoking changes numerous alveolar macrophage functions and is one of the most important risk factors for postoperative pulmonary complications. The current study tested the hypothesis that smoking impairs antimicrobial and proinflammatory responses in alveolar macrophages during anesthesia and surgery. METHOD: The authors studied 30 smoking and 30 nonsmoking patients during propofol-fentanyl general anesthesia. Alveolar immune cells were harvested by bronchoalveolar lavage immediately and 2, 4, and 6 h after induction of anesthesia and at the end of surgery. The types of alveolar immune cell and macrophage aggregation were determined. The authors measured opsonized and unopsonized phagocytosis. Microbicidal activity was determined as the ability of the macrophages to kill Listeriamonocytogenes directly. Finally, RNA was extracted from harvested cells and cDNA was synthesized by reverse transcription. The expression of interleukin 1beta, 6, and 8, interferon gamma, and tumor necrosis factor alpha were measured by semiquantitative polymerase chain reaction using beta-actin as an internal standard. RESULTS: The fraction of aggregated macrophages increased significantly over time in both groups, whereas phagocytosis of opsonized and nonopsonized particles and microbicidal activity of alveolar macrophages decreased significantly. The changes, though, were nearly twice as great as in patients who smoked. Gene expression of all proinflammatory cytokines in alveolar immune cells except interleukin 6 increased 2- to 20-fold over time in both groups. The expression of interleukin 1beta, interferon gamma, and tumor necrosis factor alpha, however, increased only half as much in smokers as in nonsmokers. CONCLUSION: Smoking was associated with macrophage aggregation but markedly reduced phagocytic and microbicidal activity-possibly because expression of proinflammatory cytokines was reduced in these patients. Our data thus suggest that smokers may have a limited ability to mount an effective pulmonary immune defense after anesthesia and surgery.

Anesthesia, General↗
PubMed2000

Supplemental intraoperative oxygen augments antimicrobial and proinflammatory responses of alveolar macrophages.

BACKGROUND: The first goal was to test the hypothesis that 100% inspired oxygen maintained for approximately 8 h intraoperatively is not associated with impaired pulmonary oxygenation. The authors also tested the hypothesis that intraoperative inhalation of 100% oxygen augments proinflammatory and antimicrobial responses of alveolar macrophages during anesthesia and surgery. METHODS: The authors studied patients administered 100% oxygen (n = 30) and 30% oxygen (n = 30) during propofol-fentanyl general anesthesia. Alveolar macrophages were harvested by bronchoalveolar lavage immediately, 2, 4, and 6 h after induction of anesthesia, and at the end of surgery. The authors measured "opsonized" and "unopsonized" phagocytosis and microbicidal activity. RNA was extracted from harvested cells and cDNA was synthesized. The expression of interleukin(IL)-1beta, IL-6, IL-8, interferon-gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) was measured by semiquantitative polymerase chain reaction. RESULTS: Gene expression of all proinflammatory cytokines except IL-6 increased fourfold to 20-fold over time in both groups. However, expression of TNF-alpha and IL-8, IFN-gamma, and IL-6 and IL-1beta was 2-20 times greater in patients administered 100% than in those administered 30% oxygen. Unopsonized and opsonized phagocytosis and microbicidal activity decreased progressively, with the decreases being nearly twice as great during inhalation of 30% oxygen versus 100% oxygen. CONCLUSION: Inhalation of 100% oxygen improved intraoperative decreases in phagocytic and microbicidal activity possibly because expression of proinflammatory cytokines was augmented. These data therefore suggest that intraoperative inhalation of 100% oxygen augments antimicrobial and proinflammatory responses in alveolar macrophages during anesthesia and surgery.

Anesthesia, Intravenous↗
PubMed2000

Acute opioid tolerance: intraoperative remifentanil increases postoperative pain and morphine requirement.

BACKGROUND: Rapid development of acute opioid tolerance is well established in animals and is more likely to occur with large doses of short-acting drugs. The authors therefore tested the hypothesis that intraoperative remifentanil administration results in acute opioid tolerance that is manifested by increased postoperative pain and opioid requirement. METHODS: Fifty adult patients undergoing major abdominal surgery were randomly assigned to two anesthetic regimens: (1) desflurane was kept constant at 0.5 minimum alveolar concentrations and a remifentanil infusion was titrated to autonomic responses (remifentanil group); or (2) remifentanil at 0.1 microg. kg-1. min-1 and desflurane titrated to autonomic responses (desflurane group). All patients were given a bolus of 0.15 mg/kg morphine 40 min before the end of surgery. Morphine was initially titrated to need by postanesthesia care nurses blinded to group assignment. Subsequently, patients-who were also blinded to group assignment-controlled their own morphine administration. Pain scores and morphine consumption were recorded for 24 postoperative h. RESULTS: The mean remifentanil infusion rate was 0.3 +/- 0.2 microg. kg-1. min-1 in the remifentanil group, which was significantly greater than in the desflurane group. Intraoperative hemodynamic responses were similar in each group. Postoperative pain scores were significantly greater in the remifentanil group. These patients required morphine significantly earlier than those in the desflurane group and needed nearly twice as much morphine in the first 24 postoperative h: 59 mg (25-75% interquartile range, 43-71) versus 32 mg (25-75% interquartile range, 19-59; P < 0.01). CONCLUSIONS: Relatively large-dose intraoperative remifentanil increased postoperative pain and morphine consumption. These data suggest that remifentanil causes acute opioid tolerance and hyperalgesia.

Analgesia, Patient-Controlled↗
PubMed2000

Core cooling by central venous infusion of ice-cold (4 degrees C and 20 degrees C) fluid: isolation of core and peripheral thermal compartments.

BACKGROUND: Central venous infusion of cold fluid may be a useful method of inducing therapeutic hypothermia. The aim of this study was to quantify systemic heat balance and regional distribution of body heat during and after central infusion of cold fluid. METHODS: The authors studied nine volunteers, each on two separate days. Anesthesia was maintained with use of isoflurane, and on each day 40 ml/kg saline was infused centrally over 30 min. On one day, the fluid was 20 degrees C and on the other it was 4 degrees C. By use of a tympanic membrane probe core (trunk and head) temperature and heat content were evaluated. Peripheral compartment (arm and leg) temperature and heat content were estimated with use of fourth-order regressions and integration over volume from 18 intramuscular thermocouples, nine skin temperatures, and "deep" hand and foot temperature. Oxygen consumption and cutaneous heat flux estimated systemic heat balance. RESULTS: After 30-min infusion of 4 degrees C or 20 degrees C fluid, core temperature decreased 2.5 +/- 0.4 degrees C and 1.4 +/- 0.2 degrees C, respectively. This reduction in core temperature was 0.8 degrees C and 0.4 degrees C more than would be expected if the change in body heat content were distributed in proportion to body mass. Reduced core temperature resulted from three factors: (1) 10-20% because cutaneous heat loss exceeded metabolic heat production; (2) 50-55% from the systemic effects of the cold fluid per se; and (3) approximately 30% because the reduction in core heat content remained partially constrained to core tissues. The postinfusion period was associated with a rapid and spontaneous recovery of core temperature. This increase in core temperature was not associated with a peripheral-to-core redistribution of body heat because core temperature remained warmer than peripheral tissues even at the end of the infusion. Instead, it resulted from constraint of metabolic heat to the core thermal compartment. CONCLUSIONS: Central venous infusion of cold fluid decreases core temperature more than would be expected were the reduction in body heat content proportionately distributed. It thus appears to be an effective method of rapidly inducing therapeutic hypothermia. When the infusion is complete, there is a spontaneous partial recovery in core temperature that facilitates rewarming to normothermia.

Adult↗
PubMed2000

Risk factors for early-onset, ventilator-associated pneumonia in critical care patients: selected multiresistant versus nonresistant bacteria.

BACKGROUND: Ventilator-associated pneumonia is the leading nosocomial infection in critically ill patients. The frequency of ventilator-associated pneumonia caused by multidrug-resistant bacteria has increased in recent years, and these pathogens cause most of the deaths attributable to pneumonia. The authors, therefore, evaluated factors associated with selected multidrug-resistant ventilator-associated pneumonia in critical care patients. METHODS: The authors prospectively recorded potential risk factors at the time of intensive care unit admission. An endotracheal aspirate was obtained in all patients who met clinical criteria for pneumonia. Patients were considered to have ventilator-associated pneumonia only when they met the clinical criteria and aspirate culture was positive for bacteria 48 h or more after initiation of mechanical ventilation. Pediatric patients were excluded. Adult patients with ventilator-associated pneumonia were first grouped as "early-onset" (< 5 days) and "late-onset," determined by episodes of ventilator-associated pneumonia, and then, assigned to four groups based on the bacteria cultured from their tracheal aspirates: Pseudomonas aeruginosa, Acinetobacter baumanii, methicillin-resistant staphylococci, and all others. The first three bacteria were considered to be multidrug resistant, whereas the others were considered to be antibiotic susceptible. Potential risk factors were evaluated with use of univariate statistics and multivariate regression. RESULTS: Among 486 consecutive patients admitted during the study, 260 adults underwent mechanical ventilation for more than 48 h. Eighty-one patients (31%) experienced 99 episodes of ventilator-associated pneumonia, including Pseudomonas(33 episodes), methicillin-resistant staphylococci (17 episodes), Acinetobacter(9 episodes), and nonresistant bacteria (40 episodes). Sixty-six of these episodes were early onset and 33 episodes were late onset. Logistic regression analysis identified three factors significantly associated with early-onset ventilator-associated pneumonia caused by any one of the multidrug-resistant bacterial strains: emergency intubation (odds ratio, 6.4; 95% confidence interval, 2.0-20.2), aspiration (odds ratio, 12.7; 95% confidence interval, 2.4-64.6), and Glasgow coma score of 9 or less (odds ratio, 3.9; 95% confidence interval, 1.3-11.3). A. baumanii-related pneumonia cases were found to be significantly associated with two of these factors: aspiration (odds ratio, 14.2; 95% confidence interval, 1.5-133.8) and Glasgow coma score (odds ratio, 6.0; 95% confidence interval, 1.1-32.6). CONCLUSIONS: The authors recommend that patients undergoing emergency intubation or aspiration or who have a Glasgow coma score of 9 or less be monitored especially closely for early-onset multidrug-resistant pneumonia. The occurrence of aspiration and a Glasgow coma score of 9 or less are especially associated with pneumonia caused by A. baumanii.

Adult↗
PubMed2000

Alfentanil reduces the febrile response to interleukin-2 in humans.

OBJECTIVE: Manifestation of intraoperative fever is impaired by volatile anesthetics and muscle relaxants. Opioids are common anesthetic adjuvants and remain the dominant treatment for postoperative surgical pain and sedation of critically ill patients. The effect of opioids on normal thermoregulatory control is well established. However, the extent to which these drugs might inhibit fever remains unknown. Accordingly, we tested the hypothesis that relatively low plasma concentrations of the mu-receptor agonist alfentanil reduce fever magnitude. DESIGN: Prospective, randomized, crossover study. SETTING: Outcomes Research Laboratory, at the Department of Anesthesia and Perioperative Care, University of California, San Francisco. PATIENTS: Eight healthy male volunteers, aged 25-31 yrs, each studied on three separate days. INTERVENTION: Each volunteer was given an intravenous injection of 30 IU/g interleukin (IL)-2, followed 2 hrs later by 70 IU/g. One hour after the second dose, the volunteers were randomly assigned to three doses of alfentanil: a) none (control); b) a target plasma concentration of 100 ng/mL; and c) a target concentration of 200 ng/mL. Opioid administration continued for 5 hrs. METHODS AND MAIN RESULTS: Alfentanil significantly reduced the febrile response to pyrogen, decreasing integrated tympanic membrane temperatures from 7.5+/-2.2 degrees C x hr on the control day, to 4.9+/-1.5 degrees C x hr with 100 ng/mL alfentanil, and to 5.1+/-1.7 degrees C x hr with 200 ng/mL alfentanil (p = .011). Peak temperatures were also significantly reduced from 38.5+/-0.4 degrees C on the control day, to 38.0+/-0.4 degrees C on the 100 ng/mL-alfentanil day and 38.0+/-0.6 degrees C on the 200-ng/mL day (p = .019). Plasma cytokine concentrations increased after IL-2 administration, roughly in proportion to the elevation in core temperature. However, cytokine concentrations did not differ significantly among the treatment groups. CONCLUSION: Alfentanil significantly reduced the febrile response to IL-2 administration. However, the reduction was comparable at plasma concentrations near 100 and 200 ng/mL. These data indicate that concentrations of opioids commonly observed in critical care patients significantly inhibit the manifestation of fever.

Adult↗
PubMed1999

Postoperative pain and subcutaneous oxygen tension.

Surgical patients randomly assigned to standard pain control had postoperative subcutaneous oxygen partial pressures that were significantly less than patients given better pain treatment. Our data suggest that control of postoperative pain is a major determinant of surgical-wound infection and should be given the same consideration as maintaining adequate vascular volume and normothermia.

Adolescent↗
PubMed1999

[Mild intraoperative hypothermia. Another risk factor for postoperative complications].

Intraoperative mild hypothermia (core temperature 35-36 degrees) is common during major surgical procedures. Recent studies have shown that hypothermia may be related to the development of postoperative serious complications such as impaired platelet function with increased blood loss and transfusion requirements, postoperative morbid cardiac events, impaired wound healing, and prolonged hospitalization. Core hypothermia during surgery should therefore receive more attention as a risk factor for postoperative complications. The most effective prevention of intraoperative hypothermia is forced air warming combined with the infusion of warm fluids. The paper gives clinical guidelines for monitoring and prevention of intraoperative core hypothermia.

Guidelines as Topic↗
PubMed1999

The effects of physical treatment on induced fever in humans.

PURPOSE: Initial treatments for fever include the amelioration of underlying causes and administration of antipyretic medications. However, patients who fail these treatments are often actively cooled, which may be counterproductive because decreasing skin temperature increases the thermoregulatory core target temperature. Cooling may also provoke metabolic and autonomic stress and thermal discomfort. SUBJECTS AND METHODS: We studied 9 subjects, each on 3 days. Fever was induced each day with 100,000 IU/kg of interleukin-2 administered intravenously (elapsed time zero). Randomly assigned treatments were 1) control (a cotton blanket), 2) cooling (forced air at 15 degrees C), or 3) self-adjust (forced-air warming adjusted to comfort). Treatments were maintained for 3 to 8 elapsed hours. RESULTS: Peak core temperatures (mean +/- SD) were 38.4 +/- 0.5 degrees C on the control day, 38.1 +/- 0.5 degrees C on the cooling day, and 38.5 +/- 0.4 degrees C on the self-adjust day. Integrated core temperatures were 6.0 +/- 1.6 degrees C x h on the control day, 5.7 +/- 2.2 degrees C x h on the cooling day, and 6.4 +/- 1.2 degrees C x h on the self-adjust day. Neither peak nor integrated core temperatures differed significantly on the 3 days. Shivering was common on the cooling day but otherwise rare. Oxygen consumption was normal on the control and self-adjust days but increased 35% to 40% during cooling (P = 0.0001). Mean arterial pressure and plasma norepinephrine and epinephrine concentrations were significantly greater during cooling (P <0.05). On a self-reported thermal comfort scale, the subjects were miserable during cooling and significantly more comfortable on the self-adjust than control day (P <0.05). CONCLUSION: We conclude that active cooling should be avoided in unsedated patients with moderate fever, because it does not reduce core temperature but does increase metabolic rate, activate the autonomic nervous system, and provoke thermal discomfort.

Adult↗
PubMed1999

Less core hypothermia when anesthesia is induced with inhaled sevoflurane than with intravenous propofol.

UNLABELLED: Hypothermia after the induction of anesthesia results initially from core-to-peripheral redistribution of body heat. Sevoflurane and propofol both inhibit central thermoregulatory control, thus causing vasodilation. Propofol differs from sevoflurane in producing substantial peripheral vasodilation. This vasodilation is likely to facilitate core-to-peripheral redistribution of heat. Once heat is dissipated from the core, it cannot be recovered. We therefore tested the hypothesis that the induction of anesthesia with i.v. propofol causes more core hypothermia than induction with inhaled sevoflurane. We studied patients undergoing minor oral surgery randomly assigned to anesthetic induction with either 2.5 mg/kg propofol (n = 10) or inhalation of 5% sevoflurane (n = 10). Anesthesia in both groups was subsequently maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe skin temperature gradients <0 degrees C were considered indicative of significant vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Patients in both groups were vasodilated throughout most of the surgery. Nonetheless, core temperatures in patients who received propofol were significantly lower than those in patients who received inhaled sevoflurane. These data support our hypothesis that even a brief period of vasodilation causes substantial redistribution hypothermia that persists throughout surgery. IMPLICATIONS: Core temperatures in patients who received i.v. propofol were consistently lower than those in patients who received inhaled sevoflurane, although anesthesia was subsequently maintained with sevoflurane in nitrous oxide in both groups. This suggests that even a brief period of propofol-induced vasodilation during anesthetic induction causes substantial redistribution hypothermia that persists throughout surgery.

Adult↗
PubMed1999

Exposure to sevoflurane and nitrous oxide during four different methods of anesthetic induction.

UNLABELLED: The National Institute for Occupational Safety and Health-recommended exposure levels for nitrous oxide exposure are 25 ppm as a time-weighted average over the time of exposure. The exposure limit for halogenated anesthetics (without concomitant nitrous oxide exposure) is 2 ppm. Inhaled sevoflurane provides an alternative to i.v. induction of anesthesia. However, the inadvertent release of anesthetic gases into the room is likely to be greater than that with induction involving i.v. anesthetics. We therefore evaluated anesthesiologist exposure during four different induction techniques. Eighty patients were assigned to one of the induction groups to receive: 1) sevoflurane and nitrous oxide from a rebreathing bag, 2) sevoflurane and nitrous oxide from a circle circuit, 3) propofol 3 mg/kg, and 4) thiopental sodium 5 mg/kg. Anesthesia was maintained with sevoflurane and nitrous oxide via a laryngeal mask. Trace concentrations were measured directly from the breathing zone of the anesthesiologist. During induction, peak concentrations of sevoflurane and nitrous oxide with the two i.v. methods rarely exceeded 2 ppm sevoflurane and 50 ppm nitrous oxide. Concentrations during the two inhalation methods were generally <20 ppm sevoflurane and 100 ppm nitrous oxide. During maintenance, median values were near 2 ppm sevoflurane and 50 ppm nitrous oxide in all groups. Sevoflurane concentrations during inhaled induction frequently exceeded the National Institute for Occupational Safety and Health-recommended exposure ceiling of 2 ppm but mostly remained <20 ppm. Exposure during the maintenance phase of anesthesia also frequently exceeded the 2-ppm ceiling. We conclude that operating room anesthetic vapor concentrations are increased during inhaled inductions and remain increased with laryngeal mask ventilation. IMPLICATIONS: We compared waste gas concentrations to sevoflurane and nitrous oxide during four different induction methods. During inhaled induction with a rebreathing bag or a circle circuit system, waste gas concentrations frequently exceed National Institute for Occupational Safety and Health limits of 2 ppm sevoflurane and 50 ppm nitrous oxide. Therefore, we recommend that people at risk (e.g., women of child-bearing age) should pay great attention when using this technique.

Air Pollution, Indoor↗
PubMed1999

Onset time, recovery duration, and drug cost with four different methods of inducing general anesthesia.

UNLABELLED: We compared two conventional induction techniques (thiopental and propofol), an inhaled induction with sevoflurane using a circle system, and a rebreathing method. Fentanyl 1 microg/kg was given to women undergoing 10- to 20-min procedures. Anesthesia was induced (n = 20 each) with one of the following: 1) sevoflurane and N2O from a rebreathing bag (Sevo/Bag). A 5-L bag was prefilled with a mixture of sevoflurane 7% and N2O 60% in oxygen. The bag was connected between the normal circle system, separated by a spring-loaded valve; 2) sevoflurane 8% and N2O 60% from a circle system on a conventional anesthesia machine with a total fresh gas flow of 6 L/min (Sevo/Circle); 3) propofol 3 mg/kg as an i.v. bolus; 4) thiopental sodium 5 mg/kg as an i.v. bolus. Postoperative nausea and vomiting was treated with ondansetron. Induction times were comparable with each method. Recovery duration was shortest with sevoflurane, intermediate with propofol, and longest with thiopental. Induction drug costs were lowest with Sevo/Bag and thiopental, intermediate with Sevo/Circle, and highest with propofol. However, sevoflurane (by either method) caused considerable nausea and vomiting that required treatment. Consequently, total drug cost was least with thiopental, intermediate with Sevo/Bag and propofol, and greatest with Sevo/Circle. Thus, no single technique was clearly superior. IMPLICATIONS: Anesthetic induction techniques influence awakening time, recovery duration, and drug costs. We tested two i.v. methods and two inhaled techniques. However, none of the four tested methods was clearly superior to the others.

Adult↗
PubMed1999

Tissue heat content and distribution during and after cardiopulmonary bypass at 17 degrees C.

UNLABELLED: We measured afterdrop and peripheral tissue temperature distribution in eight patients cooled to approximately 17 degrees C during cardiopulmonary bypass and subsequently rewarmed to 36.5 degrees C. A nasopharyngeal probe evaluated trunk and head temperature and heat content. Peripheral tissue temperature (arm and leg temperature) and heat content were estimated using fourth-order regressions and integration over volume from 30 tissue and skin temperatures. Peripheral tissue temperature decreased to 19.7+/-0.9 degrees C during bypass and subsequently increased to 34.3+/-0.7 degrees C during 104+/-18 min of rewarming. The core-to-peripheral tissue temperature gradient was -5.9+/-0.9 degrees C at the end of cooling and 4.7+/-1.5 degrees C at the end of rewarming. The core-temperature afterdrop was 2.2+/-0.4 degrees C and lasted 89+/-15 min. It was associated with 1.1+/-0.7 degrees C peripheral warming. At the end of cooling, temperatures at the center of the upper and lower thigh were (respectively) 8.0+/-5.2 degrees C and 7.3+/-4.2 degrees C cooler than skin temperature. On completion of rewarming, tissue at the center of the upper and lower thigh were (respectively) 7.0+/-2.2 degrees C and 6.4+/-2.3 degrees C warmer than the skin. When estimated systemic heat loss was included in the calculation, redistribution accounted for 73% of the afterdrop, which is similar to the contribution observed previously in nonsurgical volunteers. IMPLICATIONS: Temperature afterdrop after bypass at 17 degrees C was 2.2+/-0.4 degrees C, with approximately 73% of the decrease in core temperature resulting from core-to-peripheral redistribution of body heat. Cooling and rewarming were associated with large radial tissue temperature gradients in the thigh.

Adult↗
PubMed1999

Intraoperative phenylephrine infusion decreases the magnitude of redistribution hypothermia.

UNLABELLED: Core hypothermia during the first hour after induction of general anesthesia results largely from an internal core-to-peripheral redistribution of body heat. This redistribution results from both central inhibition of tonic thermoregulatory vasoconstriction in the arteriovenous shunt and anesthetic-induced vasodilation. We therefore tested the hypothesis that acute administration of phenylephrine, a pure alpha-adrenergic agonist, reduces the magnitude of anesthetic-induced core-to-peripheral redistribution of body heat. Patients undergoing minor oral surgery were randomly assigned to an infusion of 0.5 microgram.kg-1.min-1 phenylephrine i.v. or no treatment (control). The phenylephrine infusion was started immediately before anesthesia was induced with 2.5 mg/kg propofol i.v. Subsequently, anesthesia was maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe, skin-temperature gradients < 0 degree C were considered indicative of significant arteriovenous shunt vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Although there were no significant differences in skin-temperature gradients, core temperatures in the untreated patients decreased significantly more (1.2 +/- 0.4 degrees C) than in those given phenylephrine (0.5 +/- 0.2 degree C, P < 0.001). These data suggest that maintaining precapillary vasoconstriction of blood vessels, not in the arteriovenous shunt reduces the magnitude of redistribution hypothermia. IMPLICATIONS: Core hypothermia immediately after induction of general anesthesia results largely from core-to-peripheral redistribution of body heat. Core temperature reduction during the first hour of anesthesia decreased less in patients given phenylephrine than in untreated controls. These data suggest that maintaining precapillary vasoconstriction possibly reduces the magnitude of redistribution hypothermia.

Adrenergic alpha-Agonists↗
PubMed1999

Wound infiltration and drain lavage with ropivacaine after major shoulder surgery.

UNLABELLED: Subcutaneous infiltration and wound lavage with ropivacaine is an alternative to opioids after major shoulder surgery. However, the efficacy and potential toxicity of this method remain unclear. We therefore evaluated plasma ropivacaine concentrations after shoulder infiltration and wound lavage. We subsequently quantified the efficacy of two ropivacaine concentrations. Patients undergoing major shoulder surgery were anesthetized with alfentanil and propofol. The initial patients (n = 18) received ropivacaine 7.5 mg/mL and ropivacaine plasma concentrations were measured in 15-min intervals. The subsequent 45 patients were randomly assigned to: 1) isotonic saline, 2) 3.75 mg/mL ropivacaine, or 3) 7.5 mg/mL ropivacaine. Ten milliliters of each solution was administered subcutaneously and 20 mL was injected into the wound drain which was clamped for 10 min. Supplemental postoperative pain relief was provided by patient-controlled anesthesia using the opioid piritramid (3.5-mg boluses, 6-min lock-out). Postoperative pain scores were recorded on a 100-mm visual analog scale for 4 h in the initial patients and for 10 h in the second part of the study. Unbound ropivacaine plasma concentrations peaked after 15 min at 0.08+/-0.09 microg/mL; the maximum was 0.30 microg/mL, compared with a toxic threshold of 0.6 microg/mL. In the second part of the study, pain scores were significantly lower after 3.75 mg/mL (20+/-15 mm) or 7.5 mg/mL (10+/-9 mm) ropivacaine than saline (35+/-10 mm). Piritramid requirements differed significantly in the three groups, being highest with saline and lowest with ropivacaine 7.5 mg/mL. We conclude that wound infiltration and lavage with 30 mL ropivacaine 7.5 mg/mL after major shoulder surgery resulted in very low pain scores and opioid requirement. IMPLICATIONS: Wound infiltration and lavage with 30 mL ropivacaine 7.5 mg/mL after major shoulder surgery resulted in very low pain scores and opioid requirement.

Amides↗