摘要:

BackgroundClonidine has been added to local anesthetic regimens for various peripheral nerve blocks, resulting in prolonged anesthesia and analgesia. The authors postulated that using clonidine as a component of intravenous regional anesthesia (IVRA) would enhance postoperative analgesia.MethodsForty‐five patients undergoing ambulatory hand surgery received IVRA with lidocaine, 0.5%, and were assigned randomly and blindly to three groups. The control group received intravenous saline, the intravenous clonidine group received 1 &mgr;g/kg clonidine intravenously, and the IVRA clonidine group received 1 &mgr;g/kg clonidine as part of the IVRA solution. After their operations, the patients’ pain and sedation scores and analgesic use were recorded.ResultsPatients in the IVRA clonidine group had a significantly longer period of subjective comfort when they required no analgesics (median [range]) for 460 min (215–1,440 min), compared with 115 min (14–390 min) for the control group and 125 min (17–295 min) for the intravenous clonidine group (P< 0.0001). The patients who received IVRA with clonidine reported significantly lower pain scores 1 and 2 h after tourniquet deflation compared with the other groups, and they required no fentanyl in the postanesthesia care unit. They also required fewer analgesic tablets (325 mg acetaminophen with 30 mg codeine) in the first 24 h (2 ± 1, mean ± SD) compared with the other two groups, 5 ± 1 tablets (control) and 4 ± 2 tablets (intravenous clonidine) (P< 0.0001). No significant postoperative sedation, hypotension, or bradycardia developed in any of the patients.ConclusionThe addition of 1 &mgr;g/kg clonidine to lidocaine, 0.5%, for IVRA in patients undergoing ambulatory hand surgery improves postoperative analgesia without causing significant side effects during the first postoperative day.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundImpaired movement of the cricoarytenoid joint with hoarseness and immobility of the vocal ligament can occur as a consequence of endotracheal intubation. The biomechanics and pathomechanism of cricoarytenoid subluxation have not been demonstrated to date.MethodsThe present study attempts to simulate the trauma that has been associated with arytenoid cartilage subluxation in intubation trials on 37 unfixed larynges in cadavers from persons aged 25 to 89 years. Larynges were intubated or extubated according to former conceptions of arytenoid subluxation, which assume that the arytenoid tip enters the lumen of the tracheal tube, or that a deflection of the arytenoid occurs during withdrawal of the endotracheal tube with the cuff of the tube only partially deflated. Also, manual attempts were carried out to subluxate the arytenoid cartilage. Subsequently after dissecting the left and right cricoarytenoid joint from each larynx, the morphologic changes induced experimentally were analyzed using gross microscopic and histologic methods.ResultsWithin the scope of the experiment, it proved impossible to produce any subluxation of a cricoarytenoid joint. Histologic analysis revealed injuries of synovial folds, joint‐surface impressions of the articular cartilage, and fractures in the area of the subchondral bone in some joints.ConclusionsBased on the morphologic results, it was concluded that intubation trauma of the cricoarytenoid joint does not cause subluxationper se, but rather that formation of a hemarthros or fractures of the joint bodies lead to fixation of the joint surfaces in an abnormal position. Subsequent ankylosis may occur.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundTo study the interaction between nitrous oxide and sevoflurane during trachea intubation, the authors determined the minimum alveolar concentration of sevoflurane for tracheal intubation (MACTI) with and without nitrous oxide in children.MethodsSeventy‐two children aged 1–7 yr were assigned randomly to receive one of three end‐tidal concentrations of nitrous oxide and one of four end‐tidal concentrations of sevoflurane: 0% nitrous oxide with 2.0, 2.5, 3.0, or 3.5% sevoflurane; 33% nitrous oxide with 1.5, 2.0, 2.5, or 3.0% sevoflurane; or 66% nitrous oxide with 1.0, 1.5, 2.0, or 2.5% sevoflurane. After steady state end‐tidal anesthetic concentrations were maintained for at least 10 min, laryngoscopy and intubation were attempted using a straight‐blade laryngoscope and an uncuffed tracheal tube. The interaction between nitrous oxide and sevoflurane was investigated using logistic regression analysis of the responses to intubation.ResultsLogistic regression curves of the probability of no movement in response to intubation in the presence of sevoflurane and 0, 33, and 66% nitrous oxide were parallel. The interaction coefficient between nitrous oxide and sevoflurane did not differ significantly from zero (P= 0.89) and was removed from the logistic model. The MACTI(± SE) of sevoflurane was 2.66 ± 0.16%, and the concentration of sevoflurane required to prevent movement in 95% of children was 3.54 ± 0.25%. Thirty‐three percent and 66% nitrous oxide decreased the MACTIof sevoflurane by 18% and 40% (P< 0.001), respectively.ConclusionsWe conclude that nitrous oxide and sevoflurane suppress the responses to tracheal intubation in a linear and additive fashion in children.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundTourniquet deflation following total knee arthroplasty (TKA) frequently results in release of emboli into the pulmonary circulation. Small emboli may gain access to the systemic circulationviaa transpulmonary route or through a patent foramen ovale. This study examined the incidence of cerebral microembolism after tourniquet release by transcranial Doppler (TCD) ultrasonography and its correlation with echogenic material detected in the left atrium.MethodsTwenty‐two adult patients (9 men, 13 women) undergoing TKA were studied with simultaneous TCD ultrasonography and transesophageal echocardiography. Data were recorded after anesthesia induction and tourniquet inflation and during tourniquet deflation. Emboli counts were performed manually off‐line. Echogenic material in the left atrium was qualitatively assessed and correlated with TCD data. Patients were examined postoperatively for focal neurologic deficits.ResultsFifteen patients had unilateral TKA (six left, nine right) and seven had bilateral TKA. Cerebral emboli were detected in 9 of 15 patients (60%) with unilateral TKA and in 4 of 7 patients (57%) with bilateral TKA. Echogenic material was identified in the left atrium in eight patients (two through a patent foramen ovale and six from the pulmonary veins). Emboli counts were significantly higher in patients with bilateral TKA compared with those with unilateral TKA (P< 0.05). Duration of tourniquet time in patients with emboli was longer only during bilateral TKA (P< 0.05). All patients with echogenic material in the left atrium detected by transesophageal echocardiography had emboli as assessed by TCD ultrasonography. No focal neurologic deficits were identified.ConclusionsCerebral microembolism occurs frequently during tourniquet release, even in the absence of a patient foramen ovale. This passage most likely occurs through the pulmonary capillaries or the opening of recruitable pulmonary vessels.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundThe effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow–metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol‐induced isoelectric electroencephalogram.MethodsTwenty patients aged 20–62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 &mgr;g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End‐tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age‐adjusted 0.5 MAC (0.8–1%) or 1.5 MAC (2.4–3%) end‐tidal sevoflurane; or age‐adjusted 0.5 MAC (0.5–0.7%) or 1.5 MAC (1.5–2%) end‐tidal isoflurane. After 15 min of unchanged end‐tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels.ResultsAlthough both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4 ± 3 and 17 ± 3% at 0.5 and 1.5 MAC sevoflurane; 19 ± 3 and 72 ± 9% at 0.5 and 1.5 MAC isoflurane [mean ± SD];P< 0.05). All patients required phenylephrine (100–300 &mgr;g) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia.ConclusionsIn common with other volatile anesthetic agents, sevoflurane has an intrinsic dose‐dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundThe human immunodeficiency virus protease inhibitor ritonavir is a potent inhibitor of the cytochrome P450 3A4 enzyme, and ritonavir's concomitant administration with the substrates of this enzyme may lead to dangerous drug interactions.MethodsThe authors investigated possible interactions between ritonavir and intravenously administered fentanyl in a double‐blind, placebo‐controlled, cross‐over study in two phases. Twelve healthy volunteers received orally ritonavir or placebo for 3 days; the dose of ritonavir was 200 mg three times on the first day and 300 mg three times on the second. The last dose of ritonavir 300 mg or placebo was given on the morning of the third day. On the second day, 2 h after the afternoon pretreatment dose, fentanyl 5 &mgr;g/kg was injected intravenously in 2 min with naloxone to moderate its effects, and 15 timed venous blood samples were collected for 18 h.ResultsRitonavir reduced the clearance of fentanyl by 67% from 15.6 ± 8.2 to 5.2 ± 2.0 ml · min−1· kg−1(P< 0.01). The area under the fentanyl plasma concentration–time curve from 0 to 18 h was increased from 4.8 ± 2.7 to 8.8 ± 2.3 ng · ml−1· h−1by ritonavir (P< 0.01). Ritonavir did not affect the initial concentrations and the steady‐state volume of distribution of fentanyl. One subject discontinued participation before fentanyl administration because of severe side effects, and during the study 8 of the remaining 11 subjects reported nausea.ConclusionsRitonavir can inhibit the metabolism of fentanyl significantly, so caution should be exercised if fentanyl is given to patients receiving ritonavir medication.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundBlood pressure (BP) monitoring with arterial waveform display requires an arterial cannula. We evaluated a new noninvasive device, Vasotrac (Medwave, Arden Hills, MN) that provides BP measurements approximately every 12–15 beats and displays pulse rate and a calibrated arterial waveform for each BP measurement.MethodsSurgical and critically ill patients (n = 80) served as subjects for the study. BPs, pulse waveforms, and pulse rates measuredviaa radial artery catheter were compared with those obtained by the Vasotrac from the opposite radial artery. Data were analyzed to determine agreement between the two systems of measurement.ResultsBlood pressure measured noninvasively by the Vasotrac demonstrated excellent correlation (P< 0.01) with BP measuredviaa radial arterial catheter (systolic r2= 0.93; diastolic r2= 0.89; mean r2= 0. 95). Differences in BP measured by the Vasotracversusthe radial arterial catheter were small. The mean ± SD bias and precision were as follows: systolic BP 0.02 ± 5.4 mmHg and 3.9 ± 3.7 mmHg; diastolic BP −0.39 ± 3.9 mmHg and 2.7 ± 2.8 mmHg; mean BP −0.21 ± 3.0 mm Hg and 2.1 ± 2.2 mmHg compared with radial artery measurements. The Vasotrac pulse rates were almost identical to those measured directly (r2= 0.95). The Vasotrac BP waveform resembled those directly obtained radial artery pulsatile waveforms.ConclusionsIn surgical and critically ill patients, the Vasotrac measured BP, pulse rate, and displayed radial artery waveform, which was similar to direct radial arterial measurements. It should be a suitable device to measure BP frequently in a noninvasive fashion.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundRecently, two centers have independently developed a risk score for predicting postoperative nausea and vomiting (PONV). This study investigated (1) whether risk scores are valid across centers and (2) whether risk scores based on logistic regression coefficients can be simplified without loss of discriminating power.MethodsAdult patients from two centers (Oulu, Finland: n = 520, and Wuerzburg, Germany: n = 2202) received inhalational anesthesia (without antiemetic prophylaxis) for various types of surgery. PONV was defined as nausea or vomiting within 24 h of surgery. Risk scores to estimate the probability of PONV were obtained by fitting logistic regression models. Simplified risk scores were constructed based on the number of risk factors that were found significant in the logistic regression analyses. Original and simplified scores were cross‐validated. A combined data set was created to estimate a potential center effect and to construct a final risk score. The discriminating power of each score was assessed using the area under the receiver operating characteristic curves.ResultsRisk scores derived from one center were able to predict PONV from the other center (area under the curve = 0.65–0.75). Simplification did not essentially weaken the discriminating power (area under the curve = 0.63–0.73). No center effect could be detected in a combined data set (odds ratio = 1.06, 95% confidence interval = 0.71–1.59). The final score consisted of four predictors: female gender, history of motion sickness (MS) or PONV, nonsmoking, and the use of postoperative opioids. If none, one, two, three, or four of these risk factors were present, the incidences of PONV were 10%, 21%, 39%, 61% and 79%.ConclusionsThe risk scores derived from one center proved valid in the other and could be simplified without significant loss of discriminating power. Therefore, it appears that this risk score has broad applicability in predicting PONV in adult patients undergoing inhalational anesthesia for various types of surgery. For patients with at least two out of these four identified predictors a prophylactic antiemetic strategy should be considered.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundLike ischemic preconditioning, certain volatile anesthetics have been shown to reduce the magnitude of ischemia/ reperfusion injuryviaactivation of K+adenosine triphosphate (ATP)‐sensitive (KATP) channels. The purpose of this study was (1) to determine if ischemic preconditioning (IPC) and sevoflurane preconditioning (SPC) increase nitric oxide release and improve coronary vascular function, as well as mechanical and electrical function, if given for only brief intervals before global ischemia of isolated hearts; and (2) to determine if KATPchannel antagonism by glibenclamide (GLB) blunts the cardioprotective effects of IPC and SPC.MethodsGuinea pig hearts were isolated and perfused with Krebs–Ringer's solution at 55 mmHg and randomly assigned to one of seven groups: (1) two 2‐min total coronary occlusions (preconditioning, IPC) interspersed with 5 min of normal perfusion; (2) two 2‐min occlusions interspersed with 5 min of perfusion while perfusing with GLB (IPC+GLB); (3) SPC (3.5%) for two 2‐min periods; (4) SPC+GLB for two 2‐min periods; (5) no treatment before ischemia (control [CON]); (6) CON+GLB; and (7) no ischemia (time control). Six minutes after ending IPC or SPC, hearts of ischemic groups were subjected to 30 min of global ischemia and 75 min of reperfusion. Left‐ventricular pressure, coronary flow, and effluent NO concentration ([NO]) were measured. Flow and NO responses to bradykinin, and nitroprusside were tested 20–30 min before ischemia or drug treatment and 30–40 min after reperfusion.ResultsAfter ischemia, compared with before (percentage change), left‐ventricular pressure and coronary flow, respectively, recovered to a greater extent (P< 0.05) after IPC (42%, 77%), and treatment with SPC (45%, 76%) than after CON (30%, 65%), IPC+GLB (24%, 64%), SPC+GLB (20%, 65%), and CON+GLB (28%, 64%). Bradykinin and nitroprusside increased [NO] by 30 ± 5 (means ± SEM) and 29 ±4 nM, respectively, averaged for all groups before ischemia. [NO] increased by 26 ± 6 and 27 ± 7 nM, respectively, in SPC and IPC groups after ischemia, compared with an average [NO] increase of 8 ± 5 nM (P< 0.01) after ischemia in CON and each of the three GLB groups. Flow increases to bradykinin and nitroprusside were also greater after SPC and IPC.ConclusionsPreconditioning with sevoflurane, like IPC, improves not only postischemic contractility, but also basal flow, bradykinin and nitroprusside‐induced increases in flow, and effluent [NO] in isolated hearts. The protective effects of both SPC and IPC are reversed by KATPchannel antagonism.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundIsoflurane enhances the functional recovery of postischemic, reperfused myocardium by activating adenosine A1receptors and adenosine triphosphate–regulated potassium channels. Whether protein kinase C is involved in this process is unknown. The authors tested the hypothesis that inhibition of protein kinase C, using the selective antagonist bisindolylmaleimide, attenuates isoflurane‐enhanced recovery of stunned myocardium in dogs.MethodsFifty dogs were randomly assigned to receive intracoronary vehicle or bisindolylmaleimide (2 or 8 &mgr;g/min) in the presence or absence of isoflurane (1 minimum alveolar concentration). Five brief (5 min) coronary artery occlusions interspersed with 5‐min reperfusion periods followed by 180 min of final reperfusion were used to produce myocardial stunning. Hemodynamics, regional segment shortening, and myocardial blood flow (radioactive microspheres) were measured at selected intervals.ResultsThere were no differences in baseline hemodynamics, segment shortening, or coronary collateral blood flow between groups. Isoflurane significantly (P< 0.05) decreased heart rate, mean arterial pressure, rate pressure product, and the maximum rate of increase of left ventricular pressure (+dP/dtmax) in the presence or absence of bisindolylmaleimide. Sustained contractile dysfunction was observed in dogs that received vehicle (recovery of segment shortening to 12 ± 8% of baseline), in contrast to those that received isoflurane (75 ± 7% recovery). Bisindolylmaleimide at a dose of 2 &mgr;g/min alone enhanced recovery of segment shortening (50 ± 7% of baseline) compared with vehicle‐pretreated dogs, and isoflurane in the presence of 2 &mgr;g/min bisindolylmaleimide further enhanced recovery of contractile function (79 ± 8% of baseline). In contrast, 8 &mgr;g/min bisindolylmaleimide alone (32 ± 12%) or combined with isoflurane (37 ± 17%) did not enhance recovery of segment shortening compared with vehicle‐pretreated dogs.ConclusionsThe results indicate that protein kinase C inhibition using low doses of bisindolylmaleimide alone produces cardioprotection, and isoflurane further enhances this protection. In contrast, high doses of bisindolylmaleimide are not cardioprotective in the presence or absence of isoflurane. A role for protein kinase C during isoflurane‐induced recovery of the stunned myocardium cannot be excluded.

ISSN:0003-3022    

出版商:OVID    

年代:1999

数据来源: OVID