ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Background:Intraoperative hypothermia initially results from internal redistribution of heat facilitated by anesthesia-induced vasodilatlon. Preinductlon skin-surface warming minimizes postinduction hypothermia in anesthetized volunteers. However, its efficacy might be reduced in surgical situations, because of multiple sources of heat loss.Methods:Intraoperative core and mean skin temperatures were measured during total hip arthroplasty in 16 patients, randomly assigned to be covered preoperatlvely with a warming blanket for ≥90 min (prewarmed group) or not covered (unwarmed group).Results:During the first hour of anesthesia, core temperature decreased more than twice as much in the unwarmed group (−0.7 ± 0.1° C; mean ± SE) than in the prewarmed patients (−0.3 ± 0.1° C). At the end of surgery, core temperature was 36.3 ± 0.1° C in the prewarmed group and 35.2 ± 0.2° C in the unwarmed group. During recovery, seven patients obviously shivered in the unwarmed group and none in the prewarmed group.Conclusions:Preanesthetic skin-surface warming reduces the initial postinductlon hypothermia in surgical patients, preventing intraoperative hypothermia and postoperative shivering even for procedures lasting 3 h or longer.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Background:Core temperature decreases rapidly after induction of anesthesia, largely because heat is redistributed to peripheral tissues. The hypothesis that warming peripheral tissues before induction of general anesthesia (prewarming) minimizes hypothermia was tested. Because circulating blood volume may be greater during exposure to heat compared to cold, the hypothesis that prewarming decreases the amount of hypotension associated with induction of anesthesia was tested also. Finally, the hypothesis that the difference between direct radial arterial blood pressure and blood pressure measured oscillometrically at the brachial artery depends on thermoregulatory and anesthetic conditions was tested.Methods:Each of six volunteers underwent general anesthesia (propofol and nitrous oxide) twice on the same day. Each anesthetic lasted 1 h and was preceded by either 2 h of active warming with forced air or 2 h of passive cooling by exposure to a typical operating room environment. After induction of each anesthetic, volunteers were fully exposed to the ambient environment. Volunteers recovered for 2 h before starting the second preinduction treatment.Results:Initial tympanic membrane temperatures were similar before each preinduction treatment: 36.7 ± 0.4° C when volunteers were not warmed and 36.7 ± 0.6° C when volunteers were warmed. Tympanic membrane temperature did not change during the preinduction period without warming but increased slightly (ΔT = 0.4 ± 0.2° C) during warming. After induction of anesthesia, core temperatures decreased to 36.1 ± 0.4° C over 1 h when volunteers were prewarmed but decreased to 34.9 ± 0.4° C when they were not. Radial arterial systolic, diastolic, and mean blood pressures were lower before induction of anesthesia when volunteers were warmed compared to when no warming was given. Oscillometric diastolic and mean pressures also were lower during prewarming; however, oscillometric systolic pressure did not differ significantly. Prewarming did not result in less hypotension after induction. Without warming, the difference (radial arterial minus oscillometric) in systolic blood pressure measurements was ≈17 mmHg. Warming was associated with a reversal of the systolic pressure difference to ≈−6 mmHg. After induction of anesthesia, the differences in systolic and mean pressure measurements became more negative with respect to the preinduction values regardless of preinduction warming treatment.Conclusions:These data confirm our hypothesis that redistribution hypothermia can be minimized by preinduction warming of peripheral tissues. Prewarming decreases blood pressure but does not prevent subsequent hypotension after induction. The difference between radial arterial blood pressure and oscillometric blood pressure depends on thermoregulatory vasomotor changes but also may be influenced by vasodilation associated with administration of propofol and nitrous oxide.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Background:Increasing age appears to be associated with a slower onset of neuromuscular blockade, but such an effect has not been studied with the same doses of the same drugs across pediatric and adult age groups.Methods:The authors measured the evoked compound action potential of the adductor pollicis muscle in response to 0.1-Hz stimulation of the ulnar nerve, during fentanyl-thiopental-oxygen anesthesia, in 160 patients aged 1–3 yr, 3–10 yr, 20–40 yr, or 60–80 yr. Subparalyzlng doses of vecuronium (0.03 mg/kg) or succinylcholine (0.3 mg/kg), or paralyzing doses of vecuronium (0.1 mg/kg) or succinylcholine (1.0 mg/kg), were administered to ten patients in each age group.Results:Onset time, defined as the time from injection to maximum depression of response with a subparalyzlng dose or the time from injection to ablation of visible response with a paralyzing dose, varied with age in all groups (P< 0.001). For 0.3 mg/kg succinylcholine, it increased from 49 ± 6 s in 1–3-yr-old patients, to 104 ± 9 s in 60–80-yr-old patients (P< 0.00001). For 0.03 mg/kg vecuronium, onset time was 3.6–5.9 times longer than for succinylcholine, increasing from 219 ± 15 s in 3–10-yr-old patients to 473 ± 30 s in 60–80-yr-old patients (P< 0.00001 by linear regression). For paralyzing doses, succinylcholine 1.0 mg/kg had an onset time of 58 ± 7 s and 95 ± 7 s, in 1–3-yr-old and 60–80-yr-old patients, respectively (P< 0.001). For 0.1 mg/kg vecuronium, onset time varied between 125 ± 19 s in 1–3-yr-old patients to 295 + 31 s in 60–80-yr-old patients (P< 0.00001), and was 2.1–3.3 times longer than 1 mg/kg succinylcholine.Conclusions:Increasing age is associated with slower onset for both succinylcholine and vecuronium. When equipotent, subparalyzing doses of succinylcholine and vecuronium are compared, onset time is 4.5 times as long with vecuronium.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Background:Few studies have been reported on the direct depressive effects of sevoflurane on myocardial contractility in humans. Direct assessment of contractile state is possible by examining the slope of left ventricular end-systolic wall stress (LVESWS)versusvelocity of circumferential fiber shortening with heart rate corrected (Vcfc) relationship with echocardiography. Using this contractile index, the effects of sevoflurane/nitrous oxide were compared with that of enflurane/nitrous oxide on myocardial contractility in humans.Methods:Twenty-eight subjects were studied during either sevoflurane/nitrous oxide or enflurane/nitrous oxide anesthesia. Systolic, diastolic, and mean arterial blood pressure, heart rate, and transesophageal echocardiographic data were determined at 0.9 MAC and 1.35 MAC of sevoflurane or enflurane, both with 60% N2O, and at 1.6 MAC of sevoflurane with 60% N2O. Furthermore, another 28 awake subjects were studied with transthoracic echocardiography to examine the contractile state at awake state, and echocardiograms, heart rate, and arterial blood pressure were recorded.Results:Heart rate did not changed significantly in either group. Enflurane/nitrous oxide produced significantly greater decrease in arterial blood pressure than did sevoflurane/nitrous oxide. The Vcfc at each anesthetic dose in both anesthetic groups was significantly less than that in the awake subjects group. Sevoflurane/nitrous oxide produced no significant change in Vcfc at 1.5 MAC, whereas enflurane/nitrous oxide caused significant dose-related decrease in Vcfc. Vcfc produced by sevoflurane/nitrous oxide was significantly greater than that produced by enflurane/nitrous oxide. There was no significant difference in LVESWS (index of afterload) between the groups. With respect to the LVESWS-Vcfc relationship, myocardial contractility was significantly depressed in both the sevoflurane and the enflurane groups compared to the awake subjects group. However, myocardial contractility produced by enflurane/nitrous oxide was significantly less than that by sevoflurane/nitrous oxide at equiMAC concentration.Conclusions:The results of the present study suggest that sevoflurane has fewer depressant effects on cardiac function than does enflurane.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Background:The esophageal detector device (EDD) is a diagnostic tool for confirmation of tracheal intubation. Capnography is the accepted standard for such confirmation. The purpose of this investigation was to determine whether results using the EDD and capnography agree.Methods:Five hundred patients were divided into three separate studies. In study 1, with 300 consecutive patients, tracheal intubation was performed and tested with the EDD followed by capnography. In study 2, 100 patients had the esophagus intentionally intubated, and confirmation was tested similarly. The tube was then removed and the trachea intubated, and testing followed. Study 3 involved 100 patients and used a double-blind, randomized design. The tube was intentionally inserted into either the esophagus (n = 51) or trachea (n = 49), and testing followed.Results:In study 1, the compressed EDD bulb reinflated 270 times and always agreed with capnography; in 20 of the 270 subjects (7%) bulb reinflation was delayed, taking from 5–30 s. In 30 instances, the bulb remained compressed, and there was no capnogram indicating esophageal intubation. In study 2, regardless of esophageal or tracheal intubation, agreement between EDD and capnogram was 100%. In study 3, the agreement between the two detecting instruments was 100%, but reinflation of the EDD bulb was delayed in 4% of tracheal intubations. In the 500 patients studied, results from the EDD and capnogram always agreed, but in 6% of all tracheal intubations, the EDD bulb inflated slowly. Of 181 esophageal intubations, the results from the EDD and capnogram always agreed,i.e., there was no reinflation or capnogram. The sensitivity, specificity, and predictive value for the EDD In all of these studies was 100%.Conclusions:The EDD is a valuable diagnostic technique for confirming tracheal intubation. Results using EDD agree with results using capnography; in 6% of instances there is a slow reinflation; and where there is no capnography, such as on hospital wards, EDD may be a useful diagnostic tool.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Background:Previous studies have shown that pulse oximeters whose sensors are positioned improperly may yield erroneously low saturation (SpO2) values on normoxemic subjects. The behavior of oximeters with malpositioned sensors during hypoxemia has not been studied. The current study is aimed at determining the behavior of several different pulse oximeters over a wide range of arterial oxygen saturation (SaO2).Methods:In each of 12 healthy volunteers, a radial artery cannula was inserted, and eight different pulse oximeters, five of which had malpositioned sensors, were applied. Subjects breathed controlled mixtures of nitrogen and oxygen to slowly vary their SaO2from 100% to 70%. Arterial blood samples were analyzed and pulse oximeter data were recorded at five stable SaO2values for each subject.Results:The oximeters with malpositioned sensors vary greatly in their behavior, depending on both the actual SaO2and the manufacturer and model. One oximeter underestimated saturation at all SaO2values, while three others underestimated at high SaO2and overestimated at low SaO2. Linear regression analysis shows a decrease in the slope of SpO2versusSaO2in most cases, indicating a loss of sensitivity to SaO2changes. Between subject variation in response curves was significant.Conclusions:The calibration curves of the pulse oximeters studied were changed greatly by sensor malpositioning. At low SaO2values, these changes could cause the oximeter to indicate that a patient was only mildly hypoxemic when, in fact, hypoxemia was profound. It is recommended that sensor position be checked frequently and that inaccessible sensor locations be avoided whenever possible.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

Background:Increased postoperative platelet reactivity may contribute to arterial thrombotic complications following surgery. α2Agonists, which are being used increasingly to blunt the stress response of surgery, increase platelet aggregationin vitro. We compared perioperative changes in platelet reactivity in 21 patients receiving either clonidine or placebo.Methods:Patients undergoing major abdominal surgery were randomized to receive oral and transdermal clonidine (n = 11) or placebo (n = 10). All patients received similar perioperative management, including preoperatlve sedation, general anesthesia without neuraxial opioids, or local anesthetics and postoperative patient-controlled intravenous morphine. Blood was obtained for measurement of clonidine level, fibrinogen concentration, platelet count, and platelet reactivity (impedance aggregometry and dense granule release) before induction and 24, 48, and 72 h postoperatlvely.Results:Thirteen of the 21 patients had biopsy-proven cancer at surgery, 5 of 11 received clonidine and 8 of 10 received placebo (NS). Clonidine levels were therapeutic (1–2 ng/ml) throughout the study period. Clonidine administration had no effect on platelet count or platelet reactivity. Therefore, the groups were combined for further analysis. In this group (n = 21), compared to preoperatlve values, fibrinogen levels rose maximally (36%) at 72 h postoperatlvely and platelet counts decreased 22% at 48 h. Platelet reactivity (aggregation and degranulation) to collagen, adenosine diphosphate, arachidonic acid, and ristocetin, increased at 24, 48, and 72 h postoperatively. Thrombin-induced (supramaximal stimulus) dense granule release did not change from preoperative values.Conclusions:These data indicate that major abdominal surgery causes increased platelet reactivity postoperatively but does not effect maximal degranulation. This increased platelet reactivity occurs within 48 h of surgery, coinciding with the peak incidence of postoperative arterial thrombotic complications. Clonidine administration has no effect on surgically induced changes in platelet reactivity. In this surgical patient population, the use of clonidine should not increase the risk of platelet-induced perioperative arterial thrombosis.

ISSN:0003-3022    

出版商:OVID    

年代:1993

数据来源: OVID