摘要:

BackgroundThere is controversy about whether capnography is adequate to monitor pulmonary ventilation to reduce the risk of significant respiratory acidosis in pregnant patients undergoing laparoscopic surgery. In this prospective study, changes in arterial to end-tidal carbon dioxide pressure difference (PaCO2–-PetCO2), induced by carbon dioxide pneumoperitoneum, were determined in pregnant patients undergoing laparoscopic cholecystectomy.MethodsEight pregnant women underwent general anesthesia at 17–30 weeks of gestation. Carbon dioxide pnueumoperitoneum was initiated after obtaining arterial blood for gas analysis. Pulmonary ventilation was adjusted to maintain PetCO2around 32 mmHg during the procedure. Arterial blood gas analysis was performed during insufflation, after the termination of insufflation, after extubation, and in the postoperative period.ResultsThe mean ± SD for PaCO2–-PetCO2was 2.4 ± 1.5 before carbon dioxide pneumoperitoneum, 2.6 ± 1.2 during, and 1.9 ± 1.4 mmHg after termination of pneumoperitoneum. PaCO2andpH during pneumoperitoneum were 35 ± 1.7 mmHg and 7.41 ± 0.02, respectively. There were no significant differences in either mean PaCO2–-PetCO2or PaCO2andpH during various phases of laparoscopy.ConclusionsCapnography is adequate to guide ventilation during laparoscopic surgery in pregnant patients. Respiratory acidosis did not occur when PetCO2was maintained at 32 mmHg during carbon dioxide pneumoperitoneum.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundIn a subset of coronary surgery patients, a transient increase in cardiac load by leg elevation resulted in a decrease in maximal rate of pressure development (dP/dtmax) and a major increase in end-diastolic pressure (EDP). This impairment of left ventricular (LV) function appeared to be related to a deficient length-dependent regulation of myocardial function. The present study investigated whether analysis of transmitral flow patterns with transesophageal echocardiography constituted a noninvasive method to identify these patients.MethodsHigh-fidelity LV pressure tracings and transmitral flow signals were obtained in 50 coronary surgery patients during an increase in cardiac load by leg elevation. Using linear regression analysis, changes in transmitral E-wave velocity and deceleration time (DT) were related to changes in dP/dtmaxand EDP.ResultsChanges in dP/dtmaxwith leg elevation were closely related to corresponding changes in E-wave velocity (r = 0.81;P< 0.001) and to changes in DT (r = 0.78;P< 0.001). Similarly, changes in EDP were related to changes in E-wave velocity (r = 0.83;P< 0.001) and to changes in DT (r = 0.84;P< 0.001). The decrease in dP/dtmaxand the major increase in EDP in some patients was associated with an increase in E-wave velocity and a decrease in DT, indicating development of a restrictive LV filling pattern.ConclusionsImpairment of LV function with leg elevation was associated with the development of a restrictive transmitral filling pattern. Analysis of transmitral flow patterns by means of transesophageal echocardiography therefore allowed noninvasive identification of a subset of coronary surgery patients with impaired length-dependent regulation of LV function.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThis study determined the responses to increasing plasma concentrations of dexmedetomidine in humans.MethodsTen healthy men (20–27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml).ResultsThe initial dose of dexmedetomidine decreased catecholamines 45–76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid–base was unchanged.ConclusionsIncreasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose–response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundChanging plasma protein concentrations may affect the protein binding and pharmacokinetics of drugs in the postoperative phase. Therefore, the authors evaluated the pharmacokinetics of ropivacaine, administered by 72-h epidural infusion to provide postoperative analgesia.MethodsTwenty-eight patients, scheduled for major orthopedic surgery during combined epidural and general anesthesia received a bolus dose of ropivacaine (50 or 75 mg), followed by constant-rate (10 ml/h) epidural infusion of ropivacaine 2 mg/ml (group 1) or 3 mg/ml (group 2). Total and unbound plasma concentrations of ropivacaine and pipecoloxylidide and plasma concentrations of &agr;1-acid glycoprotein were determined. In addition, the urinary excretion of ropivacaine and major metabolites was measured.ResultsTotal plasma concentrations of ropivacaine increased steadily during the infusion, reaching 2.7 ± 0.7 and 2.9 ± 0.5 mg/l in groups 1 and 2 after 72 h constant-rate infusion. Unbound ropivacaine concentrations reached average steady state levels of approximately 0.06 and 0.07 mg/l. Total and unbound concentrations of pipecoloxylidide increased to 1.0 ± 0.4 and 0.4 ± 0.2 mg/l (group 1) and 1.2 ± 0.4 and 0.5 ± 0.1 mg/l (group 2) after 72 h infusion. &agr;1-Acid glycoprotein concentrations initially decreased, but thereafter increased steadily to approximately twice the baseline values.ConclusionsPostoperative increases in plasma &agr;1-acid glycoprotein concentrations enhance the protein binding of ropivacaine and pipecoloxylidide, causing divergence of total and unbound plasma concentrations.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundBronchospasm is a potential complication in anyone undergoing general anesthesia. Because volatile anesthetics relax bronchial smooth muscle, the effects of two newer volatile anesthetics, desflurane and sevoflurane, on respiratory resistance were evaluated. The authors hypothesized that desflurane would have greater bronchodilating effects because of its ability to increase sympathetic nervous system activity.MethodsInformed consent was obtained from patients undergoing elective surgery with general anesthesia. We recorded airway flow and pressure after thiopental induction and tracheal intubation (baseline) and for 10 min after beginning volatile anesthesia (∼ 1 minimum alveolar concentration inspired). Respiratory system resistance was determined using the isovolume technique.ResultsFifty subjects were randomized to receive sevoflurane (n = 20), desflurane (n = 20), or thiopental infusion (n = 10, 0.25 mg · kg−1· h−1). There were no differences between groups for age, height, weight, smoking history, and American Society of Anesthesiologists physical class. On average, sevoflurane reduced respiratory resistance 15% below baseline, whereas both desflurane (+5%) and thiopental (+10%) did not decrease respiratory resistance. The respiratory resistance changes did not differ in patients with and without a history of smoking during sevoflurane or thiopental. In contrast, administration of desflurane to smokers resulted in the greatest increase in respiratory resistance.ConclusionsSevoflurane causes moderate bronchodilation that is not observed with desflurane or sodium thiopental. The bronchoconstriction produced by desflurane was primarily noted in patients who currently smoked.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundRapid 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.MethodsFifty 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 &mgr;g · kg−1· min−1and 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.ResultsThe mean remifentanil infusion rate was 0.3 ± 0.2 &mgr;g · kg−1· min−1in 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)versus32 mg (25–75% interquartile range, 19–59;P< 0.01).ConclusionsRelatively large-dose intraoperative remifentanil increased postoperative pain and morphine consumption. These data suggest that remifentanil causes acute opioid tolerance and hyperalgesia.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe combined spinal–epidural (CSE) technique using bupivicaine–fentanyl has become an established method of pain control during parturition. One limitation is the relatively short duration of effective analgesia produced by bupivicaine–fentanyl. In contrast, subarachnoid meperidine has been shown to provide a long duration of anesthesia in nonobstetric patients. Therefore, the authors tested the hypothesis that subarachnoid meperidine produces a significant increase in the duration of analgesia compared with bupivicaine–fentanyl.MethodsBased on a power analysis of preliminary data, the authors intended to recruit 90 patients for the study, randomized to three groups: 2.5 mg bupivicaine–25 &mgr;g fentanyl, 15 mg meperidine, or 25 mg meperidine. However, after enrolling 34 patients, the study was discontinued because of a significant increase in nausea or vomiting in the study patients.ResultsNausea or vomiting was substantially increased in both meperidine groups compared with the bupivicaine–fentanyl group: 16 with nausea or vomiting in the meperidine groups (n = 21), compared with 1 in the bupivicaine–fentanyl group (n = 11), P = 0.0011. The mean duration of analgesia provided by 25 mg meperidine was 126 ± 51 min, compared with 98 ± 29 min for bupivicaine–fentanyl and 90 ± 67 min for 15 mg meperidine. These data were not significant (P= 0.27).ConclusionsAlthough intrathecal meperidine could potentially prolong subarachnoid analgesia during labor, its use was associated with a significant incidence of nausea or vomiting. These data do not support the use of subarachnoid meperidine in doses of 15 or 25 mg for labor analgesia.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

MethodsThe authors studied two groups of sheep with lung injury produced by saline lavage. In the first group, 0, 5, 10, and 20 ppm of inhaled NO were administered in a random order before and after an intravenous Zaprinast infusion (2 mg/kg bolus followed by 0.1 mg · kg−1· min−1). In the second group, inhaled NO was administered at the same concentrations before and after an intravenous infusion of Zaprinast solvent (0.05 m NaOH).ResultsAfter lavage, inhaled NO decreased pulmonary arterial pressure and resistance with no systemic hemodynamic effects, increased arterial oxygen partial pressure, and decreased venous admixture (allP< 0.05). The intravenous administration of Zaprinast alone decreased pulmonary artery pressure but worsened gas exchange (P< 0.05). Zaprinast infusion abolished the beneficial ability of inhaled NO to improve pulmonary gas exchange and reduce pulmonary artery pressure (P< 0.05vs.control).ConclusionsThis study suggests that nonselective vasodilation induced by intravenously administered Zaprinast at the dose used in our study not only worsens gas exchange, but also abolishes the beneficial effects of inhaled NO.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundAlthough reduction of cerebral metabolic rate is thought to contribute to anesthetic neuroprotection, histologic evidence to support this concept has not been provided. In this study, histologic outcome was evaluated in rats subjected to different durations of severe forebrain ischemia while anesthetized with volatile anesthetics that have substantially different effects on cerebral metabolic rate.MethodsNormothermic rats that underwent fasting were anesthetized with 0.75 minimum alveolar concentration (MAC) isoflurane–60% nitrous oxide (N2O) or 0.75 MAC halothane–60% N2O. Ischemia was induced with use of a combination of bilateral carotid occlusion and controlled hypotension. Rats in the isoflurane group were subjected to 6.5 min or 8.0 min ischemia, whereas the halothane group received 6.5 min ischemia. Histologic damage was assessed 4 days later.ResultsWith 6.5 min ischemia, mean ± SD, hippocampal CA1 percent of dead (% dead) neurons was reduced with isoflurane–N2O (45 ± 18) versus halothane–N2O (60 ± 23,P= 0.023). Eight minutes of ischemia increased % dead neurons in the isoflurane–N2O group (60 ± 17,P= 0.017). There was no difference between the isoflurane 8.0-min and halothane 6.5-min groups (P= 0.935). A similar pattern was observed in hippocampal CA4 and the neocortex. Striatal damage was not affected by anesthetic or ischemic duration.ConclusionsAt 6.5 min ischemia, isoflurane provided improved outcomeversushalothane. Previous research has shown that 0.75 MAC isoflurane–N2O increases the time to onset of ischemic depolarization by 1.5 min and reduces cerebral metabolic rate by 42%versus0.75 MAC halothane–N2O. In the current study, when the duration of ischemia was increased by 1.5 min in the isoflurane–N2O group, histologic outcome became similar to that in halothane–N2O-anesthetized rats. These results provide evidence that cerebral metabolic rate reduction has an advantageous effect on outcome from severe brain ischemia, but also suggest that such benefit is likely to be small.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID

摘要:

BackgroundThe objective was to investigate the effects of propofol anesthesia on the pulmonary vascular response to endothelium-dependent and -independent vasodilators, compared with the responses measured in the conscious state.MethodsTwenty-six conditioned, male, mongrel dogs were instrumented long-term to measure the left pulmonary vascular pressure–flow relation. Pressure–flow plots were measured on separate days in conscious and propofol-anesthetized (5.0 mg/kg plus 0.5 mg · kg−1· min−1intravenously) dogs at baseline, after preconstriction with the thromboxane mimetic U46619, and during the cumulative intravenous administration of endothelium-dependent (acetylcholine and bradykinin) and -independent (proline–nitric oxide) vasodilators.ResultsPropofol had no effect on the baseline pressure–flow relation compared with the conscious state. A lower (P< 0.05) dose of U46619 was necessary to achieve the same degree of preconstriction during propofol anesthesia. The pulmonary vasodilator responses to bradykinin and proline–nitric oxide were similar in the conscious and propofol-anesthetized states. In contrast, the pulmonary vasodilator response to acetylcholine was markedly attenuated (P< 0.01) during propofol anesthesia. The intralipid vehicle for propofol had no effect on the acetylcholine dose–response relation.ConclusionThese results suggest that propofol causes a specific defect in the signal transduction pathway for acetylcholine-induced pulmonary vasodilation. This defect involves the endothelial and not the vascular smooth muscle component of the response.

ISSN:0003-3022    

出版商:OVID    

年代:2000

数据来源: OVID