Propofol anesthesia for major thoracic surgery

One hundred patients undergoing elective thoracic surgery were anesthetized with propofol as a continuous intravenous infusion. In 60 patients, nitrous oxide was used for supplementation. The technique proved satisfactory, but induction of anesthesia was associated with significant decreases in blood pressure. The use of nitrous oxide markedly reduced the propofol requirements, and prolonged the time to the first spontaneous breath during recovery. The mean infusion rate of propofol was 7.2 ± 2.72 mg/kg/h with air-oxygen, and 5.7 ± 1.97 mg/kg/min with nitrous oxide-oxygen (P < 0.01). This technique seems to be a satisfactory alternative for patients primarily requiring an intravenous anesthetic during thoracic surgery.     

婴儿先天性心脏病手术的麻醉处理(附93例报告)

本文报道1990年5月至1996年5月施行的93例婴儿先天性心脏病手术的麻醉处理。患儿平均月龄8．66±3．42个月，平均体重7．52±1．97公斤。麻醉诱导主要采用氯胺酮760±2．60mg/Kg肌注，静注芬太尼13．59±6．00μg／Kg，潘库溴铵0．17±0．07mg／Kg后行气管内插管。麻醉维持则采用大剂量芬太尼（41．17±16．90μ／Kg）为主的静脉复合麻醉，收到了较理想的效果。     

Cardiovascular effects of a nifedipine infusion during fentanyl-nitrous oxide anesthesia in dogs

The hemodynamic effects of a nifedipine infusion were investigated in eight dogs given fentanyl/ pancuronium/nitrous oxide/oxygen anesthesia. Nifedipine (20 μg/kg) was given intravenously over two minutes immediately prior to each 30-minute infusion at 2 μg/kg/min, 4 μg/kg/min, and 6 μg/ kg/min. The range of plasma nifedipine levels obtained was 52.1 to 113.7 ng/mL. The predominant hemodynamic effects were significant reductions systemic vascular resistance (SVR) and mean aortic pressure (MAP), accompanied by a rise in cardiac index and heart rate (HR). Administration of calcium chloride (20 mg/kg) after the nifedipine infusion had no effect on SVR or MAP, but HR was significantly reduced. Serum epinephrine and norepinephrine levels increased after the infusion of nifedipine and suggested that fentanyl did not completely overcome the sympathetic response to the profound vasodilatation. The resulting tachycardia in combination with diastolic hypotension from nifedipine could have a detrimental effect on the myocardial oxygen balance.     

Influence of high-dose opioid anesthesia on posterior tibial nerve somatosensory cortical evoked potentials: Effects of fentanyl,sufentanil, and alfentanil

The effects of high doses of fentanyl (group F), sufentanil (group S), and alfentanil (group A) on posterior tibial nerve somatosensory cortical evoked potentials were studied in 30 patients scheduled for elective valve replacement surgery. Anesthesia was induced with either fentanyl, 75 μg/kg, sufentanil, 5 μg/kg, or alfentanil, 125 μg/kg. The lungs were ventilated with oxygen/air. A bolus dose of fentanyl, 25 μg/kg, was given 30 minutes after induction of anesthesia in group F. Anesthesia was maintained with a continuous infusion of sufentanil, 5μg/kg/h, in group S, or alfentanil, 500 μg/kg/h, in group A. Latencies of the peaks of the primary cortical complex (P1, N1, 132) increased by 1 to 2 ms after induction of anesthesia, although this was significant (P < 0.01) only for P1 and N1 in groups F and S. N2 latency increased significantly (P < 0.01) by 6 to 10 ms in all groups. P1-N1 amplitude did not change after induction of anesthesia. N1-P2 amplitude decreased significantly (P < 0.01) to 60%–70% of preinduction values in groups F and S. P2-N2 amplitude decreased significantly (P < 0.01) to 60%–70% of preinduction values in all groups. P1, N1 and P2 latencies did not change significantly from the post-induction values in the period preceding cardiopulmonary bypass (75 ± 16 minutes) in groups F and S. In group A significant changes were observed only for N1 and P2 latency (P < 0.01). During this period there was a further gradual increase in N2 latency and amplitudes remained stable, except P1-N1 amplitude in group F, which decreased significantly (P < 0.05). A bolus dose of fentanyl, 25 μg/kg, given in group F at 30 minutes after induction of anesthesia did not change latencies and amplitudes. No significant differences in latency or amplitude were found at any time among the three study groups. It is concluded that anesthesia with high doses of fentanyl, sufentanil, or alfentanil is a suitable technique when intraoperative monitoring of posterior tibial nerve somatosensory cortical evoked potentials is indicated.     

A randomized double-blind comparison of fentanyl- and sufentanil-oxygen anesthesia for abdominal aortic surgery

Twenty-four patients undergoing abdominal aortic surgery for aneurysm or occlusive vascular disease entered a randomized, double-blind protocol comparing high-dose narcotic anesthesia with fentanyl (125 μg/kg) or sufentanil (25 μg/kg). All patients received perioperative β-adrenergic blockade therapy. Hemodynamic and electrocardiographic (leads 11 and V₅) responses to induction, intubation, skin incision, aortic cross-clamping, and declamping were studied. Sufentanil produced a transient decrease in mean arterial pressure and a significant reduction of systemic vascular resistance during induction. However, no significant hemodynamic differences were observed between the two groups during intubation, or at any other time during surgery. To maintain mean arterial pressure within 20% of the awake control value, the fentanyl group required an average infusion of 1.0 ± 1.1 μg/kg/min of nitroglycerin compared with 1.7 ± 2.8 μg/kg/min for the sufentanil group. Low-dose isoflurane was required in 30% of patients in the fentanyl group, compared with 41 % of the sufentanil group, for control of blood pressure. The multiple-bolus technique of narcotic administration resulted in a wide but parallel range of plasma concentrations from induction to the end of surgery with both narcotics. Mean plasma fentanyl concentrations varied between 7.2 ± 1.4 ng/mL and 26.5 ± 7.9 ng/mL, and mean sufentanil plasma concentrations varied between 1.0 ± 0.1 ng/mL and 10.6 ± 7.2 ng/mL throughout surgery. Within this range of narcotic serum levels, the authors were unable to identify a specific threshold level for either narcotic above which hemodynamic responses were consistently attenuated. A low incidence (4.5%) of intraoperative myocardial ischemia was observed. It is concluded that sufentanil and fentanyl are not different at blunting hemodynamic responses during aortic surgery. When supplemented by low doses of nitroglycerin and isoflurane, both narcotics provide anesthesia characterized by good hemodynamic control and a low incidence of myocardial ischemia.     

Comparison of the hemodynamic and echocardiographic effects of sufentanil,fentanyl, isoflurane,and halothane for pediatric cardiovascular surgery

Sufentanil, fentanyl, halothane, and isoflurane were compared as sole anesthetic agents in 48 infants and children aged 6 months to 9 years, undergoing repair of congenital heart defects. Patients were randomly assigned to receive sufentanil, 20 μg/kg, fentanyl, 100 μg/kg, isoflurane, 1.6%, or halothane, 0.9%, along with pancuronium, 0.08 mg/kg, for induction and maintenance of anesthesia. Cardiovascular function was measured by echocardiography prior to induction, postinduction, and postintubation. Systemic arterial pressure and heart rate were also recorded. Left ventricular ejection fraction (LVEF) decreased following induction with each agent: sufentanil 9%, fentanyl 9%, isoflurane 4%, and halothane 8%. Following intubation LVEF increased in the sufentanil, fentanyl, and isoflurane groups, but LVEF remained 13% below baseline values in the halothane group. Five of the 12 patients in the halothane group had a LVEF less than 55%. Arterial pressure immediately prior to bypass was significantly less than baseline in each group; however, arterial pressure was higher in the narcotic groups during isolation and cannulation of the great vessels. It is concluded that halothans, 0.9%, used as an induction agent in infants and children undergoing cardiac surgery causes a clinically significant decrease in LVEF. Based on the echocardiographic data, sufentanil, fentanyl, and isoflurane as used in the present study do not have a clinically significant effect on cardiac function and may offer an advantage to infants and children with marginal cardiovascular reserve.     

Cardiovascular effects of large doses of pentamorphone in the dog

The cardiovascular effects of large doses of pentamorphone were evaluated in nine mongrel dogs basally anesthetized with sodium thiopental, 25 to 30 mg/kg, intravenously. All dogs were mechanically ventilated with 100% oxygen, and the PaCO₂ was maintained between 35 and 40 mm Hg. Mean arterial pressure (MAP), central venous pressure, heart rate (HR), cardiac output (CO), pulmonary artery pressure, and pulmonary artery occluded pressure were measured, and stroke volume and systemic and pulmonary vascular resistances were calculated. Baseline measurements were obtained, then pentamorphone, 10 μg/mL, was given as an intravenous infusion at 2.5μg/kg/min. Additional data were obtained after infusion of 25,50, 75,100,125, 150, 200, 250, 300, and 350 μg/kg of pentamorphone. The inspired gases were then changed to 50% nitrous oxide in oxygen, and after a 20-minute equilibration period, an additional set of data was collected. Pentamorphone, 25 μg/kg, decreased HR 50%, MAP 65%, and CO 54%. No further changes in any measured or calculated variables were observed with additional doses of pentamorphone. The addition of 50% nitrous oxide to the inspired gas mixture had no effect on any measured or calculated hemodynamic variable. The minimal hemodynamic effects of pentamorphone in the dog suggest that further investigation into its use as an anesthetic is warranted.     

Dopamine counteracts hypertension during general anesthesia and hypotension during combined thoracic epidural anesthesia for abdominal aortic surgery

The influence of the degree of sympathetic nervous system activation on the cardiovascular effects of dopamine was studied during abdominal aortic surgery in 13 patients. The arterial plasma norepinephrine concentration (NE) was used as an index of sympathetic nervous system activity. During anesthesia with nitrous oxide and fentanyl, 7 patients (group 1) had a NE above 700 pg/mL and an increased mean arterial pressure (MAP) compared with the preanesthetic level (150 ± 6 v 117 ± 10 mm Hg; p < 0.01, mean ± SEM). The other 6 patients (group 2) had no significant change in MAP compared with the preanesthetic MAP (119 ± 7 v 105 ± 4 mm Hg). Dopamine, 4 μg/kg/min, decreased MAP in group 1 by 19% (150 ± 6 to 121 ± 8 mm Hg; P < 0.05) because of a 32% ± 9% decrease (P < 0.05) in systemic vascular resistance. MAP was not altered by dopamine in group 2 (119 ± 7 v 123 ± 6 mm Hg; not significant). Following termination of dopamine, the anesthetic was supplemented with thoracic epidural anesthesia (TEA). This reduced MAP to 65 ± 7 mm Hg (P < 0.01) and 56 ± 3 mm Hg(P < 0.01), and NE to 441 ± 76 (P < 0.05) and 235 ± 45 pg/mL (P < 0.05) in groups 1 and 2, respectively. During TEA, dopamine increased MAP similarly in both groups, to 85 ± 7 mm Hg (P < 0.01) and 82 ± 9 mm Hg (P < 0.05), respectively. In conclusion, dopamine, at the same dosages, counteracted hypertension during general anesthesia and counteracted hypotension during general anesthesia combined with TEA.     

Abnormal prolactin responsivity to dopaminergic suppression in hyperprolactinemic patients

Previous in vivo studies have shown that the constant infusion of dopamine suppresses prolactin (PRL) levels to within the normal range in a variety of hyperprolactinemic states, but there are no data on the relative suppressibility of the lactotroph in patients with hyperprolactinemia or on their metabolism of dopamine. Consequently, six patients with elevated PRL levels received a dopamine infusion of 4 μg/kg/min to study PRL clearance while another eight patients underwent a graded infusion at rates of 0, 1, 2 and 4 μg/kg/min to test PRL suppressibility. In four patients of the latter group an 8 μg/kg/min infusion rate was added. Healthy volunteer control subjects underwent comparable studies. PRL was measured by radioimmunoassay and dopamine by radioenzymatic techniques.The absolute PRL levels at each infusion rate were greater in the patients than in the control subjects. During the 4 μg/kg/min infusion rate, the respective PRL concentrations were 8.2 ± 1.8 and 2.0 ±0.1 ng/ml, (p < 0.001), despite higher dopamine levels in the patients (45.5 ± 6.7 versus 33.5 ± 3.8 ng/ml, p < 0.05). Neither increasing the infusion rate to 8 μg/kg/min nor prolonging the 4 μg/kg/min infusion for 6 hours decreased PRL levels further (9.6 ± 3.3 and 10.8 ± 2.5 ng/ml, respectively). Relative PRL resistance to dopamine in the hyperprolactinemic patients was demonstrated by (1) a significantly more shallow slope of the regression line of PRL versus dopamine concentrations and (2) the concentration of dopamine causing 50 percent PRL suppression (14.7 versus 6.8 ng/ml, p < 0.02). PRL metabolism was not disordered in the patients with elevated PRL levels, since the half-life ($\text{t}\text{1}\text{2}$) of the early phase of PRL clearance during their prolonged 4 μg/kg/min dopamine infusion was similar to that present in the control subjects (58.5 ± 5.9 versus 53.7 ± 9.4 min). Thus, these data demonstrate both an absolute and relative lactotroph refractoriness to dopamine in hyperprolactinemic states and suggest that there remains either a dopamine-resistant cell population, and/or continued PRL release from an enlarged cell mass, despite maximal inhibitory dopamine concentrations.     

Comparative effects of dobutamine and amrinone on coronary blood flow in patients with idiopathic dilated cardiomyopathy

Although amrinone has favorable hemodynamic effects in patients with congestive heart failure, little is known about its effects on coronary blood flow (CBF). We compared the effects of intravenous low-dose dobutamine and amrinone on CBF in 10 patients with dilated cardiomyopathy using a Doppler guidewire. We infused dobutamine at a dose of 5 and 10 μg/kg/min for 5 min. After the end of each stage, coronary flow velocity (CFV) and coronary arterial diameter (CAD) in the proximal left anterior descending coronary artery, and hemodynamic variables were obtained. After the CFV and hemodynamics returned to baseline, we infused 1 mg/kg of amrinone over 5 min, and obtained these variables at 5 and 10 min after the cessation of the infusion. CAD did not increase with dobutamine, but significantly increased after amrinone (% increase: 10 ± 7%; P < 0.001 vs. baseline). CFV progressively increased with dobutamine (5 μg/kg/min: 21 ± 26%; P < 0.05 vs. baseline; 10 μg/kg/min: 53 ± 42%; P < 0.005 vs. baseline and 5 μg/kg/min), but slightly decreased after amrinone (−4 ± 17%; P = not significant vs. baseline). CBF increased during dobutamine (5 μg/kg/min: 25 ± 29%; P < 0.05; 10 μg/kg/min: 66 ± 55%; P < 0.005) and after amrinone (19 ± 22%; P < 0.05) compared to that at baseline. Although there was a significant correlation between the percent increase in CFV and that in dP/dt during dobutamine infusion (r = 0.82, P < 0.001), this correlation was not observed after amrinone (r = 0.23). In conclusion, although both agents significantly increased CBF in patients with dilated cardiomyopathy, they do so by different mechanisms. Amrinone mainly increases CBF by causing dilatation of epicardial coronary arteries. These results suggest that amrinone has beneficial effects on coronary flow dynamics in dilated cardiomyopathy. Cathet. Cardiovasc. Diagn. 41:157–163, 1997. © 1997 Wiley-Liss, Inc.     

Effect of oral administration of lipids with 67% medium chain triglycerides on glucose homeostasis in preterm neonates

Since hypoglycemic responses to medium chain triglycerides (MCT) have been reported in adults we studied the effect of an acute oral load of lipids (2,8 g/kg) with 67% MCT on glucose homeostasis in 21 preterm infants in comparison to 14 age-matched control preterm infants. A hyperglycemic response from (mean ± SEM) 57 ± 1.1 to 74 ± 2.5 at 30 min (p < 0.01) and to 80.5 ± 2.5 mg/dl at 60 min (p < 0.01) was observed after administration of the lipids whereas no change in plasma glucose concentration was observed in the control group. After administration of the lipids there was no change in the concentration of insulin and glucagon in plasma. An intravenous glucose tolerance test (1 g/kg) was similar in the control group and 60 min after administration of the lipids. After administration of the lipids free fatty acid concentration remained unchanged while a significant decrease from 304 ± 56 to 199 ± 28 μEq/l was observed in 60 min in the control group. At 60 min β-hydroxybutyrate concentration was higher after lipid administration (630 ± 86 μmol/l) than in the control group (436 ± 66 μmole/l) (p < 0.05). A more rapid decrease in blood lactate concentration was found after lipid administration than in the control group while no change in plasma alanine concentration was observed in either groups. In five additional preterm infants, plasma glucose concentration increased from 56 ± 0.6 to 75 ± 0.9 mg/dl (p < 0.01) 60 minutes after gastric administration of glycerol (0.3 g/kg). These data show that in preterm infants, a lipid load with 67% TCM produces a hyperglycemic response through gluconeogenesis without changing the peripheral rate of glucose disappearance.     

依托咪酯静脉不同速度输注对胸科手术患者麻醉诱导期肌阵挛的影响

目的:研究依托咪酯麻醉诱导期静脉不同速度输注,对胸科手术患者肌阵挛的影响。方法:选择全身麻醉下行胸科手术男性患者90例,随机分为3组,在麻醉诱导期首先以不同的速度静注0.3 mg/kg的依托咪酯。V200组30例,输注速度为200μg/s;V400组30例,输注速度为400μg/s;V800组30例,输注速度为800μg/s。3组患者均在入睡后静注肌松剂和芬太尼镇痛。记录各组在开始静注依托咪酯即刻(T0)、停止注药时(T1)及停止注药后2 min(T2)的平均动脉压(MAP)、心率(HR)和经皮脉搏氧饱和度(SpO2)等参数、输注时间以及T0至T2期间是否发生肌阵挛及其程度。结果:3组肌阵挛发生率分别为3.3%、33.3%及73.3%,各组间比较差异均有统计学意义(P<0.05)。3组患者间肌阵挛程度分级比较,V200组,低于V400组低于V800组,差异均有统计学意义(P<0.05)。且V200组和V400组程度以1级为主,而V800组程度以3级为主。HR和SpO2值在组间和组内各时点比较差异均无统计学意义。MAP值分别在T1、T2时点组间比较V800组均低于V200组,差异均有统计学意义(P<0.05),V400组和V800组MAP值分别在组内比较T1、T2时点均明显低于T0点,差异均有统计学意义(P<0.05)。结论:减慢依托咪酯的输注速度,可以明显降低肌阵挛的发生率及肌阵挛的程度,合理的输注速度还可以避免依托咪酯对平均动脉压的降低。     

Hemodynamic effects of a lorazepam-fentanyl anesthetic induction for coronary artery bypass surgery

Previous anesthetic induction techniques using the combination of a benzodiazepine (midazolam or diazepam) and fentanyl have been reported to produce marked hypotension. In this study, anesthesia was induced with a combination of lorazepam and fentanylin in patients undergoing coronary artery bypass graft surgery. In 10 patients, anesthesia was induced using an exponentially declining continuous infusion of lorazepam equivalent to a total infused dose of 0.1 mg/kg over 15 minutes, which was supplemented at 10 minutes by fentanyl, 75 μg/kg, given as an infusion over 5 minutes. In 8 additional patients, anesthesia was induced with an exponentially declining infusion of fentanyl to a total dose of 75 μg/kg over 15 minutes, which was supplemented at 10 minutes by lorazepam, 0.1 mg/kg, given as an infusion over 5 minutes. Hemodynamics were recorded during a 20-minute observation period. One patient in each group required treatment for bradycardia during the initial drug infusion (before the second drug was added). Four additional patients in the group receiving lorazepam followed by fentanyl required treatment for bradycardia or hypotension within 10 minutes of the beginning of the fentanyl infusion. When an infusion of lorazepam was added to the fentanyl infusion, hemodynamics remained stable; however, the reverse order produced a high level of bradycardia and hypotension.     

A new dosing regimen for esmolol to treat supraventricular tachyarrhythmia in Chinese patients

Objective. The purpose of this study was to find a safe dosing regimen for esmoiol infusion to rapidly control supraventricular tachyarrhymia after cardiac surgery to Chinese patients.Background. Tachycardia increase cardiac work but reduces myocardial perfusion. Thus, in the critical period immediately after cardiac surgery, tachycardia itself warrants urgent intervention. Esmolol an ultrashort-acting beta-adrenergic blocking agent, has been reported In western published reports to have good remits and few side effects In the treatment of supraventricular tachyarrhythmia. However, its clinical application in Chinese patients has not yet been reported.Methods. When supraventricular tachyarrhymia with a rapid ventricular response (>110/min) was found early after surgery esmolol infusion with a different dosing regimen was used to control the tachyarrhythmia.Results. With the dosing regimen recommended in western published reports (repeated loading infusion with stepwise increment), acute hypotension with systolic pressure <80 mm Hg occurred in all ste patients after 1 min of loading infusion of esmolol (500 μg/kg body weight per min). To avoid the aforementioned complications, a new dosing regimen was constructed. The initial infusion rate of esmolol was set at 150 or 100 μg/kg per min, depending on the patient's age and blood pressure. When the desired heart rate was achieved, the initial infusion rate was reduced to the maintenance infusion rate to maintain the therapeutic effect [Maintenance infusion rate = Initial infusion rate x (1 − e^−0.077t), where t is the time period in minutes required by the initial infusion of esmolol to achieve the therapeutic effect]. With this new dosing regimen, tachycardia in most patients (9 of 11) could be controlled within 10 mm, and no one experienced the side effect of hypotension. The maintenance infusion rate of esmolol needed to control supraventricular tachyarrhythmia in our patients was only 73 ± 42 μg/kg per min (mean ± SD), much less than that noted hi western reports.Conclusions. The dosing reghnen for esmolol infusion recommended in western studies is not suitable for Chinese patients. In this report we propose a new dosing regimen for esmolol infusion that is both safe and rapid in the treatment of supraventricular tachyarrhythmia in Chinese patients.     

Intravenous esmolol for the treatment of supraventricular tachyarrhythmia: Results of a multicenter,baseline-controlled safety and efficacy study in 160 patients

Efficacy and safety of esmolol in the treatment of supraventricular tachyarrhythmias (SVT) was evaluated in this open-label, baseline-controlled, multicenter study. One hundred sixty patients with SVT received an intravenous infusion of esmolol in doses ranging from 25 to 300 μg/kg/min for up to 24 hours. All of the 160 patients were evaluated for safety, and 147 of them were eligible for evaluation of therapeutic response. Therapeutic response was defined as ≥ 15% reduction in the average baseline heart rate or conversion to normal sinus rhythm. Seventy-nine percent (116 of 147) of the patients exhibited a therapeutic response. The cumulative percentage response increased significantly with increasing esmolol doses up to 200 μg/kg/min. The mean (±SEM) dose of esmolol producing a therapeutic response was 97.2 ± 5.5 μg/kg/min. Among all patients (n = 160), 39% exhibited hypotension. In 58% of these patients, hypotension resolved with or without adjustment of the esmolol dose while the infusion continued; among almost all of the remaining patients, hypotension resolved within 30 minutes after esmolol was discontinued. Most patients at risk for adverse effects during beta blockade (i.e., those with diabetes mellitus, congestive heart failure, asthma, etc.) tolerated esmolol therapy, and there were no clinically important trends among the reported changes in laboratory variables. The results of the study indicate that esmolol is effective and well tolerated for the treatment of SVT.     

先天性心脏病手术两种麻醉药物的比较

目的:通过观察心内直视手术中,舒芬太尼或瑞芬太尼复合七氟烷快通道麻醉对婴幼儿血流动力学,及对术后拔管时间,术后躁动情况和ICU逗留时间的影响。方法: 2011年2月~2012年3月择期行单纯房间隔缺损或室间隔缺损修补术患儿132（男70,女62）例,年龄8个月～5岁,术前NYHA心功能Ⅰ～Ⅱ级。随机分为两组,舒芬太尼组（n=66）和瑞芬太尼组（n=66）。两组均用咪唑安定和维库溴铵诱导麻醉, 舒芬太尼组诱导用舒芬太尼1 μg/kg,术中维持持续泵入舒芬太尼2～2.5 μg/（kg·h）;瑞芬太尼组诱导用瑞芬太尼2 μg/kg,术中维持持续泵入瑞芬太尼0.1～1 μg/（kg·min）维持麻醉,两组均吸入七氟烷,持续泵入维库溴铵80～120 μg/（kg·h）。观察两组患者术前、术中、术后血流动力学变化,分别记录患儿闭眼入睡(基础,T0)、气管插管后(T1)、切皮(T2)、劈胸骨(T3)、开始转机(T4)、转机10 min(T5)、复温5 min(T6)、停机即刻(T7)、停机10 min(T8)、穿钢丝(T9)、手术结束(T10)和拔除气管插管时(T11)的心率（HR）、血压、脑电双频指数（BIS）及术后清醒时间、拔管时间、术后躁动情况和ICU逗留时间的影响。手术结束至拔除气管插管间时间为拔管时间。结果: 与T0 比较,两组患者T8、T9、 T10、T11 HR明显增快（P<0.05）,T1、T5、T6、T8平均血压（MAP）下降（P<0.05））;苏醒情况:舒芬太尼组清醒时间、拔管时间较瑞芬太尼组长（P<0.01）,瑞芬太尼组躁动发生率较舒芬太尼组高（P<0.05）。结论: 舒芬太尼或瑞芬尼复合七氟烷静吸复合麻醉用于婴幼儿单纯ASD或VSD等心内直视手术具有血流动力学稳定,能有效抑制应激反应,术后能早期拔管等特点,均能为婴幼儿先天性心脏病手术提供安全、快捷的快通道麻醉。     

Comparative cardiac effects of intravenous bolus of ipratropium bromide (itrop) and atropine sulfate in 22 patients

At the present time, there is no satisfactory pharmacological treatment for arrhythmia or conduction disorders induced by or aggravated by vagal hypertonia. The limited duration of action of the atropine derivatives currently available justifies the development of new compounds with expected longer acting duration. The aim of this study was to compare the effects of a single blind intravenous injection of ipratropium bromide to those of atropine sulfate in 22 patients. These patients were studied with continuous Holter recordings for three days. During the second and the third nights (patient sleeping), boluses of atropine (0.03 mg/kg) and of ipratropium bromide (0.03 mg/kg), respectively, were added to a continuous saline intravenous infusion. Accurate ECG analysis allowed determination of maximal heart rate peak, timing of maximal heart rate, variations in sinus cycle length, atrioventricular conduction, and durations of drug action. A nonsuggestive questionnaire was presented to patients to detect possible occurrence of side effects. The mean maximal heart rate rose significantly (p less than 0.001) for atropine (+46.2%) and for ipratropium bromide (+57.4%). The effects obtained with ipratropium bromide on the heart rate lasted nearly twice as long as those obtained with atropine (respectively, 120 +/- 38.4 min and 70 +/- 30 min- for the pharmacological half-life). Common minor muscarinic side effects (dryness of the mouth) were noted with the two drugs. In conclusion, this comparative intraindividual study confirmed the prolonged vagolytic effects of intravenous ipratropium bromide, which may be valuable in the treatment of patients with vagally mediated automaticity and conduction disturbances.     

Effects of Prolonging Peak Dobutamine Dose During Stress Echocardiography

Objectives. This study sought to test whether the physiologic advantage of a prolonged dobutamine stage during stress echocardiography can be effectively combined with a clinically practical infusion protocol.Background. Dobutamine has a half-life of 2 min and requires up to 10 min to achieve steady state. Despite these known pharmacodynamics, dobutamine stress echocardiography is routinely performed by advancing doses at 3-min intervals. Canine studies have shown that dobutamine stress echocardiography end points will occur at a lower dose if each stage is prolonged, but these findings have yet to be used in the clinical setting.Methods. The standard 3-min dobutamine dose stage during stress echocardiography was modified by extending the peak dose (40 μg/kg body weight per min) for an additional 2 min. Consecutive patients underwent this modified protocol to test whether the requirement for atropine could be reduced. According to this modified protocol, if a dobutamine stress echocardiographic end point (85% of maximal predicted heart rate, new wall motion abnormalities, hypotension, arrhythmia or intolerable symptoms) was not reached at 3 min of the peak dose, this dose was prolonged for an additional 2 min. If a dobutamine stress echocardiographic end point was still not attained, atropine (up to 1.0 mg intravenously) was administered.Results. The study included 84 patients, 22 of whom (26.2%) achieved a dobutamine stress echocardiographic end point using the standard 3-min stage. Of the 62 patients who did not reach an end point in the initial 3 min of peak dobutamine dose, the additional 2 min of dobutamine increased heart rate (from 99.6 ± 23.8 to 107.2 ± 23.2 beats/min, p < 0.01) and allowed 20 patients (32.3%, p < 0.01) to attain an end point. Of the remaining 42 patients, 23 never achieved a stress echocardiographic end point, despite 1.0 mg of atropine. One patient developed supraventricular tachycardia during the additional 2 min of dobutamine, and one developed nonsustained ventricular tachycardia after receiving atropine.Conclusions. These data demonstrate that a significant number of patients (32%) who do not reach a dobutamine stress echocardiographic end point with the standard protocol can safely attain an end point solely by extending the duration of the peak dose. Adoption of this strategy may reduce the need for supplemental atropine and its potential adverse effects.(J Am Coll Cardiol 1997;29:526–30)     

Effect of long chain triglyceride infusion on glucose metabolism in man

The effect of long chain triglyceride infusions (Intralipid 20%, 1 ml/min) on total body glucose uptake, glucose oxidation and glucose storage was examined in 25 healthy young volunteers by employing the euglycemic insulin clamp technique in combination with indirect calorimetry. Insulin was infused at three different rates (0.5, 2 and 4 mU/kg min) to achieve steady state hyperinsulinemic plateaus of 60 ± 4, 170 ± 10 and 420 ± 15 μU/ml. Prior to Intralipid infusion, the mean basal plasma free fatty acid concentration of all subjects was 385 ± 8 μmole/l. Following 90 min Intralipid infusion, the mean plasma free fatty acid level was increased to 760 ± 20 μmole/l (p < 0.001). At each insulin dose level, hyperlipidemia caused a significant reduction in total glucose uptake (5.9–3.5, 9.9–7.1, 11.1–8.8 mg/kg min, all p < 0.001. The decrease in total body glucose uptake was reflected by a decrease in both total glucose oxidation (2.4–1.6, 3.4–2.2, 3.7–2.8 mg/kg min, all p < 0.001) and glucose storage (3.6–1.9, 6.5–4.9, 7.4–5.9 mg/kg min, all p < 0.001). Basal glucose oxidation (1.3 ± 0.1 mg/kg min) fell by about 30% following 90 min of Intralipid infusion (0.9 ± 0.1 mg/kg min). Six additional subjects were studied with a lower infusion rate of Intralipid (0.5 ml/min). In these studies, insulin was infused at two different doses (0.5 and 2 mU/kg min) to achieve steady state plasma levels of 62 ± 2 and 171 ± 4 μU/ml. Intralipid caused again a significant reduction in total body glucose uptake during both the low (5.9 to 4.5 mg/kg min, p < 0.001) and the high (9.9–8.7 mg/kg min, p < 0.01) insulin clamp studies. This decrease in total glucose uptake was again the combined effect of an inhibition of both glucose storate (p < 0.05) and glucose oxidation (p < 0.001). In both high and low dose Intralipid infusion protocols, a strong inverse correlation was noted between the plasma free fatty acid concentration during the insulin clamp study and total body glucose uptake (r = 0.92, p < 0.001), glucose oxidation (r = 0.95, p < 0.001), and glucose storage (r = 0.90, p < 0.01). These results indicate that the inhibitory effect of free fatty acids on glucose utilization involves the biochemical pathways regulating both glucose oxidation and glycogen synthesis.     

瑞芬太尼对中老年人心率及心率变异性的影响

目的: 观察瑞芬太尼对不同年龄组患者心率及心率变异性的影响,以及阿托品对心率的保护作用。方法: 选择行择期手术的全麻患者,先按年龄分组:中年(M,40～59岁)和老年(O,≥60岁),每一组又随机分为单纯应用瑞芬太尼(R)组和阿托品(A)预处理,共分为4个组（每组20例）:中年单纯瑞芬太尼组（RM）、老年单纯瑞芬太尼组（RO）、中年阿托品预处理组（ARM）和老年阿托品预处理组（ARO）。RM组和RO组静脉恒速泵入瑞芬太尼2 μg/kg,泵速为1 μg/(kg·min)。其余两组患者给药方式相同,只是在静脉应用瑞芬太尼之前30 min肌肉注射阿托品0.5 mg。记录用药前（T0）、用药后1 min(T1)、2 min(T2)、3 min(T3)、5 min(T5)、7 min(T7)等各时间点的心率(HR)、低高频比值(LF/HF)。结果: RM组和RO组患者的HR、LF/HF值在T1~T7各时间点,与T0相比均降低(P<0.05);而ARM组患者给药后的各时间点的HR、LF/HF值与T0相比较,未出现有统计学意义的变化;ARO组的HR和LF/HF值在给药后也出现有统计学意义的下降（P<0.05）,但与RO组相比,下降的幅度较小。结论: 静脉泵入瑞芬太尼时,中老年患者心率及心率变异性明显降低,而阿托品可以拮抗瑞芬太尼减慢心率的作用,因此瑞芬太尼应用于中老年患者时,提倡预先应用阿托品以预防心动过缓。