Haemodynamic effects of induction of general anaesthesia with propofol during epidural anaesthesia

PURPOSE: To clarify whether propofol administration during thoracic or lumbar epidural anaesthesia intensifies the haemodynamic depression associated with epidural anaesthesia. METHODS: Patients (n = 45) undergoing procedures of similar magnitude were randomly divided into three study groups: a control group (n = 15) receiving general anaesthesia alone and two study groups undergoing thoracic (n = 15) and lumbar epidural anaesthesia (n = 15) before induction of general anaesthesia. All patients received 2 mg.kg-1 propofol at a rate of 200 mg.min-1, followed by a continuous infusion of 4 mg.kg-1.hr-1. Mean arterial blood pressure (MAP) and heart rate (HR) were measured at baseline, three minutes after induction, and one minute after tracheal intubation in all three groups and at 20 min after epidural anaesthesia was established in the thoracic and lumbar groups. RESULTS: Following epidural anaesthesia, MAP decreased from 94 +/- 14 (SD) at baseline to 75 +/- 11 mmHg (P < 0.0001) in the thoracic group and from 92 +/- 12 to 83 +/- 15 mmHg in the lumbar group. After propofol administration, MAP decreased further in the thoracic group to 63 +/- 9 mmHg (P = 0.0077) and to 67 +/- 10 mmHg (P = 0.0076) in the lumbar group. The MAP following propofol induction in the thoracic group (P < 0.0001) and in the lumbar group (P = 0.0001) was lower than MAP in the control group (81 +/- 9 mmHg). HR decreased only in response to thoracic epidural anaesthesia (P = 0.0066). CONCLUSION: The hypotensive effects of propofol are additive to those of epidural anaesthesia, resulting in a profound decrease in mean arterial pressure.     

Propofol-nitrous oxide anesthesia enhances the heart rate response to intravenous isoproterenol infusion

Heart rate (HR) response to IV atropine is attenuated during propofol-nitrous oxide (N(2)O) anesthesia. We studied the effects of propofol-N(2)O anesthesia on isoproterenol-induced HR changes. The control group (n = 15) received no propofol and no N(2)O. Patients in the propofol-N(2)O group (n = 21) received IV propofol 2.5 mg/kg over 1 min followed by a continuous infusion of propofol 10 mg x kg(-1) x h(-1). After tracheal intubation, anesthesia was maintained with propofol 5 mg. kg(-1) x h(-1) and 67% N(2)O in oxygen. All patients in both groups received IV isoproterenol at incremental infusion rates (2.5, 5, 7.5, 10, 12.5, 15, and 17.5 ng x kg(-1) x min(-1) for 2 min at each dose) until HR increased more than 20 bpm from baseline values. At the end of each infusion period, hemodynamic data were collected. The HR response to isoproterenol 7.5 ng. kg(-1) x min(-1) was increased more in the propofol group than in the control group (20 +/- 5 versus 14 +/- 4 bpm; P < 0.05). During the isoproterenol infusion at 10 ng. kg(-1) x min(-1), HR increased by more than 20 bpm in all patients in the propofol group but in only 31% of patients in the control group (P < 0.0001). These results suggest that continuous isoproterenol infusion might be useful when a large dose of atropine is ineffective in restoring normal HR during propofol-N(2)O anesthesia. IMPLICATIONS: We demonstrated that the heart rate response to IV isoproterenol infusion is enhanced during propofol-nitrous oxide anesthesia. This suggests that continuous isoproterenol infusion may be useful when a large dose of atropine is ineffective for restoration of normal heart rate in patients receiving propofol-nitrous oxide anesthesia.     

喉罩与气管插管在全麻或复合硬膜外阻滞时的心率和血压改变

目的比较喉罩与气管插管用于全麻或全麻复合硬膜外阻滞患者的HR和BP变化.方法妇科手术80例,随机分为全麻气管插管(T)组、全麻喉罩(L)组、硬膜外阻滞 全麻气管插管(ET)组、硬膜外阻滞 全麻喉罩(EL)组,每组20例.硬膜外阻滞用1%利多卡因 0.15%丁卡因.全麻诱导咪唑安定2 mg、芬太尼0.2 mg、丙泊酚1.5 mg/kg、琥珀胆碱1.5 mg/kg后插气管导管或喉罩.全麻维持50%N2O O2 异氟醚,静注阿曲库铵、芬太尼.于麻醉前(基础,入室静卧10 min后)、插管后1 min、切皮、进腹探查后5 min、拔管后1 min记录MAP、SpO2、HR、PETCO2.结果插管时HR和MAP均低于基础值,而两组喉罩HR低于插气管导管者,硬膜外复合全麻喉罩组MAP低于气管插管组.切皮时两组全麻MAP高于复合硬膜外组.探查时两组复合硬膜外者HR和MAP均低于基础值,且MAP低于单纯全麻者(P＜0.05).拔管时各组HR均显著高于基础值,MAP未复合硬膜外者显著高于基础值.结论(1)插喉罩对BP和HR的影响不如气管导管剧烈;(2)复合硬膜外阻滞时气管插管或喉罩置入应激反应轻,也可减轻探查时的BP波动.     

The effect of remifentanil on cerebral blood flow velocity in children anesthetized with propofol

BACKGROUND: Cerebrovascular stability and rapid anesthetic emergence are desirable features of a neuroanesthetic regimen. In this randomized crossover study the effect of a low-dose remifentanil infusion on cerebral blood flow velocity (CBFV) in children anesthetized with propofol was evaluated. METHODS: Twenty healthy children aged 1-6 years undergoing urological surgery were enrolled. Following face mask induction with sevoflurane, anesthesia was maintained with a standardized propofol infusion. Rocuronium was used to facilitate tracheal intubation and normothermia, and normocapnia were maintained. All children received a caudal epidural block, and a transcranial Doppler probe was placed to measure middle cerebral artery blood flow velocity (Vmca). Each patient received a remifentanil regimen of 0.5 microg x kg(-1) followed by 0.2 microg x kg(-1) x min(-1) in a predetermined order of remifentanil + propofol or propofol alone. Vmca, mean arterial pressure (MAP) and heart rate (HR) were recorded simultaneously at equilibrium with and without remifentanil. RESULTS: The combination of remifentanil and propofol caused an 8.1% decrease in MAP (P = 0.0005) and an 11.8% decrease in HR (P < 0.0001) compared with propofol alone. Vmca was not different between the two groups (P = 0.4041). CONCLUSION: The addition of remifentanil to propofol anesthesia in children causes a reduction in MAP and HR without affecting CBFV. This may imply that cerebral blood pressure autoregulation is preserved in children under propofol and remifentanil anesthesia.     

Effects of continuous infusion of landiolol on the hemodynamic response to tracheal intubation

BACKGROUND:The clinical effect of continuous infusion of landiolol with buprenorphine and lidocaine was evaluated for its effects an attenuating the cardiovascular responses to endotracheal intubation. METHODS: Tracheal intubation was performed by the same anesthesiologist after induction of anesthesia with propofol, ketamine, midazolam, buprenorphine and lidocaine, followed by administration of vecuronium, and continuous infusion of saline (Group C; n = 20) or landiolol 0.02 (Group L 2; n = 25) or landiolol 0.04 mg x kg(-1) x min(-1) (Group L4; n = 22). Heart rate (HR), systolic (sBP) and diastolic blood pressure (dBP) were recorded just before induction of anesthesia, just after and 10 min after tracheal intubation. RESULTS: Just after tracheal intubation, HR in the Groups C and L 2, but not in the group L 4, increased significantly from the baseline. Just after the tracheal intubation, sBP in the Group L 2 decreased from the baseline, and 10 min after intubation sBP in all groups decreased significantly from the baseline. Just after tracheal intubation, dBP in all groups was unchanged, and dBP in the Groups C and L 4 decreased from the baseline 10 min after the intubation. CONCLUSIONS: Continuous infusion of landiolol 0.04 mg x kg(-1) x h(-1) with buprenorphine and lidocaine can completely attenuate the hemodynamic response to tracheal intubation.     

Intravenous anesthesia with propofol in intracranial surgery]

OBJECTIVES: To analyze the repercussions of intravenous anesthesia with propofol as the single hypnotic drug on intracranial pressure (ICP) and cerebral perfusion pressure (CPP), and also to study the time until recovery from anesthesia and to tracheal extubation as well as intraoperative hemodynamic changes in patients undergoing surgery to remove a supratentorial brain tumor. PATIENTS AND METHODS: Twenty-three ASA I/II patients scheduled for exeresis of a supratentorial brain tumor were studied. A fiberoptic sensor placed in direct contact with the dura mater was used to measure ICP. Anesthetic induction was achieved with propofol (2 mg/kg). Propofol (12 and 9 mg/kg/h for 10 min and 6 mg/kg/h throughout the rest of the operation) was used for maintenance. Mean arterial pressure (MAP), heart rate (HR), ICP and CPP were recorded at baseline and 1, 2, 3 and 4 min after induction, during laryngoscopy and tracheal intubation; 1, 3, 5, 10, 15 and 20 min after tracheal intubation (L + 1, L + 3, L + 5, L + 10, L + 15, L + 20), upon placement of a craniostat; upon skin incision; upon withdrawal of propofol perfusion; and during extubation. The following variables were recorded after awakening: time until eye opening after receiving a verbal command, time until extubation and time until orientation. Analysis of variance for repeated measures (ANOVA) was performed on the results. RESULTS: MAP decreased significantly from baseline at the following times: during the post-induction period, upon placement of the craniostat, upon skin incision and when the propofol infusion was switched off. HR increased significantly during laryngoscopy and at the following moments: intubation, post intubation (L + 1, L + 3, L + 5), craniostat placement, and extubation. ICP was lower throughout the surgical period except during laryngoscopy, when this variable increased significantly. CPP decreased significantly after induction and returned to baseline after intubation. CPP was significantly higher after surgery. Recovery times after weaning from propofol infusion until eye opening in response to an order and until orientation were 13 +/- 3 and 22 +/- 4 min, respectively. The mean interval between withdrawal of propofol until extubation was 18 min. CONCLUSIONS: Intravenous anesthesia with propofol in intracranial surgery (supratentorial tumors) affords hemodynamic stability and lowers ICP except during laryngoscopy. Early recovery from anesthesia allows for neurological assessment and vigilance during the immediate postoperative period.     

Fentanyl pretreatment does not impair the reliability of an epinephrine-containing test dose during propofol-nitrous oxide anesthesia.

We designed this study to determine the hemodynamic responses to and the efficacy of a simulated IV test dose during propofol anesthesia based on the conventional heart rate (HR; positive if increase > or =20 bpm), the modified HR (positive if increase > or =10 bpm), and the systolic blood pressure (SBP; positive if increase > or =15 mm Hg) criteria. Eighty healthy patients were randomized to receive 2 mg/kgpropofol or propofol plus fentanyl (100 microg) at the induction of anesthesia (n = 40 each). After endotracheal intubation, anesthesia in both groups was maintained with propofol 8 mg x kg(-1) x h(-1) and 67% nitrous oxide in oxygen. Each group of patients was further divided into a test dose group receiving 1.5% lidocaine 3 mL plus epinephrine 15 microg (1:200,000) or a saline group (n = 20 each) receiving 3 mL of isotonic sodium chloride solution i.v. HR and SBP were monitored for 4 min after the i.v. injection of the study drug. The i.v. injection of the test dose produced a HR increase > or =20 bpm in 20 and 17 patients in the propofol and propofol-fentanyl groups, respectively, whereas all patients receiving the test dose and none receiving saline had HR increases > or =10 bpm. Therefore, in the propofol-fentanyl group, sensitivity, specificity, positive predictive value, and negative predictive value were 85%, 100%, 100%, and 87% according to the conventional HR criterion, and all were 100% according to the modified HR criterion. In the propofol group, 100% efficacy was obtained based on both HR criteria. However, all patients receiving the test dose and none receiving saline developed a SBP increase > or =15 mm Hg, resulting in 100% efficacy based on the conventional SBP criterion in both groups. Our results indicate that both the modified HR criterion and the SBP criterion are clinically applicable during propofol anesthesia with or without supplemental fentanyl. IMPLICATIONS: To determine whether an epidural catheter is in a blood vessel, an epidural test dose containing 15 microg of epinephrine is used. We found that, during propofol anesthesia with or without fentanyl, a heart rate increase > or =10 bpm and a systolic blood pressure increase > or =15 mm Hg are reliable indicators for detecting accidental intravascular injection.     

Reducing cardiovascular responses to laryngoscopy and tracheal intubation: a comparison of equipotent doses of tramadol, nalbuphine and pethidine, with placebo

The stress response to tracheal intubation may be obtunded by opioids given with induction of anesthesia. Tramadol is an opioid acting on mu-receptors and the monoaminergic pain modulating systems. This study examined vasomotor responses to tracheal intubation after equipotent doses of tramadol, nalbuphine and pethidine (3.0, 0.3 mg/kg(-1), and 1.5 mg/kg(-1), respectively), and placebo, given prior to induction of anesthesia in 118 healthy patients. Premedication and induction of anesthesia were standardized. Recordings of HR and SAP were made prior and subsequent to induction of anesthesia, and at 1, 3, 5 and 7 minutes after tracheal intubation. Prior to laryngoscopy and intubation, HR increased in all groups (p < or = 01, all comparisons), but least so after nalbuphine, whilst SAP remained unchanged after placebo, tramadol and pethidine, but fell after nalbuphine (p < 0.025). Maximum increases in HR (p < or = 0.005, all comparisons) and SAP (p < or = 0.02, all comparisons) occurred one minute after intubation. Maximum HR after placebo (108 SD 15 bpm), tramadol (107 SD 20 bpm), pethidine (113 SD 16 bpm) and nalbuphine (110 SD 26 bpm) was similar; with placebo HR remained faster than baseline until the seventh minute but had returned to baseline by the fifth minute with the opioids. Maximum SAP with tramadol (151 SD 26 mmHg) was similar to that with placebo (157 SD 20 mmHg), but was greater than after pethidine (136 SD 27 mmHg; p < 0.05) and nalbuphine (135 SD 19 mmHg; p < 0.02). With each test drug SAP returned to baseline by the third minute. It is concluded that, in these doses, 1) tramadol does not attenuate the chronotropic nor the inotropic response to tracheal intubation, and 2) pethidine and nalbuphine reduce only the inotropic response to airway instrumentation.     

A dopamine infusion decreases propofol concentration during epidural blockade under general anesthesia

PURPOSE: It is common clinical practice to use dopamine to manage the reduction in blood pressure accompanying epidural blockade. As propofol is a high-clearance drug, propofol concentrations can be influenced by cardiac output (CO). The purpose of the present study was to investigate the effects of dopamine infusions on propofol concentrations administered by a target-controlled infusion system during epidural block under general anesthesia. METHODS: 12 patients undergoing abdominal surgery were enrolled in this study. Anesthesia was induced with propofol and vecuronium 0.1 mg.kg(-1), and maintained using 67% nitrous oxide, sevoflurane in oxygen and constant infusion of propofol. Propofol was administered to all subjects via target-controlled infusion to achieve a propofol concentration at 6.0 microg.mL(-1) at intubation and 2.0 microg.mL(-1) after intubation. Before and after the administration of 10 mL of 1.5% mepivacaine from the epidural catheter and dopamine infusion at 5 microg.kg(-1).min(-1), CO and effective liver blood flow (LBF) were measured using indocyanine green. Blood propofol concentration was also determined using high-performance liquid chromatography. RESULTS: At one hour after epidural block and dopamine infusion, CO was significantly increased from 4.30 +/- 1.07 L.min(-1) to 5.82 +/- 0.98 L.min(-1) (P < 0.0001), and effective LBF was increased 0.75 +/- 0.17 L.min(-1) to 0.96 +/- 0.18 L.min(-1) (P < 0.0001). Propofol concentration was significantly decreased from 2.13 +/- 0.24 microg.mL(-1) to 1.59 +/- 0.29 microg.mL(-1) (P < 0.0001). CONCLUSIONS: Propofol concentrations decrease with an increase in CO, suggesting the possibility of inadequate anesthetic depth following catecholamine infusion during propofol anesthesia.     

丙泊酚对颅内手术麻醉诱导期脑脊液压力的影响

目的　观察丙泊酚对颅内手术病人麻醉诱导时脑脊液压力 (CSFP)、脑灌注压 (CPP)、MAP和HR的影响 ,探讨其在神经外科麻醉中的应用价值。方法　 2 0例ASAⅠ～Ⅱ级颞叶肿瘤择期手术病人 ,入室后行L3～ 4蛛网膜下隙穿刺置管监测CSFP。麻醉诱导气管内插管后 ,吸入异氟醚维持。持续监测并记录麻醉诱导中、静注芬太尼 2 μg/kg和咪唑安定 0 0 4～ 0 0 5mg/kg、静注丙泊酚2mg/kg后 2分钟、5分钟及追加丙泊酚 1mg/kg后 2分钟、5分钟和 10分钟的CSFP、MAP、HR、SpO2 、PETCO2 。结果　静注丙泊酚 2mg/kg 2分钟后CSFP较麻醉前显著下降 (P <0 0 5 ) ,5分钟和追加丙泊酚 1mg/kg后 2分钟 (气管插管时 )、5分钟时CSFP较麻醉前下降更为显著 (P <0 0 1)。MAP在静注丙泊酚 2mg/kg后 2分钟、5分钟和追加丙泊酚 1mg/kg后 2分钟、5分钟都较麻醉前明显下降 (P <0 0 5和P <0 0 1)。CPP在静注丙泊酚 2mg/kg后 2分钟和 5分钟均较麻醉前显著下降(P <0 0 1和P <0 0 5 )。HR在静注丙泊酚后较麻醉前仅有轻度降低。结论　静注丙泊酚能降低CSFP、MAP和CPP ,抑制插管反应 ,其程度与剂量相关 ,丙泊酚是颅内手术麻醉的较好选择。     

Terlipressin-ephedrine versus ephedrine to treat hypotension at the induction of anesthesia in patients chronically treated with angiotensin converting-enzyme inhibitors: a prospective, randomized, double-blinded, crossover study

In patients chronically treated with angiotensin converting-enzyme inhibitors (ACEI), typically selected doses of ephedrine do not always restore arterial blood pressure when anesthesia-induced hypotension occurs. We postulated that the administration of terlipressin, an agonist of the vasopressin system, with ephedrine more effectively restores pressure in this setting than the administration of ephedrine alone. This prospective, randomized, cross-over, double-blinded study compared terlipressin combined with ephedrine (n = 19) with ephedrine alone (n = 21) in treating hypotension at the induction of anesthesia in 40 ACEI-treated patients undergoing hypotension (mean arterial blood pressure [MAP] <65 mm Hg or <30% of baseline value) after standardized anesthetic protocol (target-controlled IV anesthesia with propofol). Data are mean +/- SD. Patient characteristics, MAP, and heart rate before and after the induction of anesthesia during hypotensive episodes were not significantly different between the two groups. After the first bolus, MAP was significantly greater in the Terlipressin-Ephedrine group (72 +/- 12 mm Hg versus 65 +/- 8 mm Hg, P < 0.05). The occurrence of a second hypotensive episode (5% versus 71%, P < 0.001), the duration (2 +/- 1 min versus 3 +/- 1 min, P < 0.01) of hypotensive episodes, and the median dose of ephedrine (3 versus 6 mg, P < 0.05) were significantly less in the Terlipressin-Ephedrine group. In conclusion, terlipressin combined with ephedrine is more effective than ephedrine alone for treating anesthesia-induced hypotension in ACEI-treated patients. We conclude that this patient population with a partially blocked endogenous response to hypotension may be good candidates for successful use of a vasopressin analog to counteract intraoperative refractory hypotension. IMPLICATIONS: Vascular surgical patients chronically treated with drugs that inhibit the functioning of the renin-angiotensin system may experience hypotension unresponsive to conventional therapy. This double-blinded, cross-over study demonstrated that in these patients the use of a vasopressin analog, terlipressin given with ephedrine, was effective in reversing intraoperative systemic hypotension refractory to ephedrine.     

阿片类药物用于抑制气管内插管副反应时合理给药时机优于药物种类和剂量的选择

已经证明芬太尼能很好地抑制气管插管的心血管副反应。舒芬太尼是芬太尼的N-4噻吩基衍生物,与阿片受体的亲和力较芬太尼强,镇痛作用是芬太尼的10倍,而且作用持续时间也更长。瑞芬太尼是一种新型μ阿片受体激动剂,具有起效迅速、作用时间短、镇痛作用与芬太尼近似、恢复迅速、无     

Propofol is superior to thiopental for intubation without muscle relaxants

PURPOSE: To compare intubating conditions and cardiovascular changes following induction of anesthesia and tracheal intubation in patients receiving either lidocaine-remifentanil-propofol or lidocaine-remifentanil-thiopental prior to induction. METHODS: In a randomized, double-blind study 76 healthy adult patients were assigned to one of two groups: lidocaine 1.5 mg.kg(-1), remifentanil 2 mug.kg(-1) and propofol 2 mg.kg(-1) (Group P) or lidocaine 1.5 mg.kg(-1), remifentanil 2 mug.kg(-1) and thiopental 5 mg.kg(-1) (Group T). Ninety seconds after the administration of the hypnotic agent, laryngoscopy and tracheal intubation were attempted. Intubating conditions were assessed as excellent, good or poor on the basis of ease of ventilation, jaw relaxation, position of the vocal cords, and patient's response to intubation and slow inflation of the tracheal cuff. The mean arterial pressure (MAP) and heart rate (HR) were measured 45 sec after hypnotic agent administration, immediately after tracheal intubation, two and five minutes after intubation. RESULTS: Excellent intubating conditions were obtained in 84% of Group P patients and 50% of Group T patients (P < 0.05). The percentage decrease from baseline MAP was significantly higher in Group P than in Group T postinduction (27.4% +/- 11.6 vs 21.8% +/- 10.0) and immediately postintubation (19.0% +/- 16.7 vs 11.2% +/- 14.9). The percentage change from baseline HR was significantly higher in Group P than in Group T postinduction (13.8% +/- 9.7 vs 0.5% +/- 12.4), immediately postintubation (8.7% +/- 13.7 vs 2.1% +/- 13.1), and two minutes postintubation (7.04% +/- 14.3 vs 3.5% +/- 14.3). CONCLUSION: Lidocaine-remifentanil-propofol is superior to lidocaine-remifentanil-thiopental for tracheal intubation without muscle relaxants. However, it induces more hypotension and bradycardia.     

The effect of remifentanil on the bispectral index change and hemodynamic responses after orotracheal intubation

In order to examine whether changes in the bispectral index (BIS) may be an adequate monitor for the analgesic component of anesthesia, we evaluated the effect of remifentanil on the BIS change and hemodynamic responses to laryngoscopy and tracheal intubation. Fifty ASA physical status I patients were randomly assigned, in a double-blinded fashion, to one of five groups (n = 10/group) according to the remifentanil target effect compartment site concentration (0, 2, 4, 8, or 16 ng/mL). The target-controlled infusion (TCI) of remifentanil was initiated 3 min after the TCI of propofol that was maintained at the effect-site concentration of 4 microg/mL throughout the study. After the loss of consciousness and before the administration of vecuronium 0.1 mg/kg, a tourniquet was applied to one arm and inflated above the systolic blood pressure in order to detect any gross movement within the first minute after tracheal intubation, which was performed 3 min after remifentanil TCI began. A BIS value was generated every 10 s. Arterial blood pressure and heart rate (HR) were measured every minute, noninvasively. Measures of mean arterial pressure (MAP), HR, and BIS were obtained before the induction, before the start of remifentanil TCI, before laryngoscopy, and 5 min after intubation. The relationships between remifentanil effect-site concentrations and BIS change or hemodynamic responses (changes in MAP and HR) to intubation were determined by logarithmic regression. BIS values were not affected by remifentanil before laryngoscopy. During this period, MAP and HR decreased significantly (P < 0.01) in the remifentanil 8 and 16 ng/mL groups. Changes in BIS, MAP, and HR were negatively correlated with remifentanil effect-site concentration (P < 0.0001). The number of movers in the remifentanil 0-, 2-, 4-, 8-, and 16-ng/mL groups was, respectively, 10, 9, 7, 1, and 0. Hypotensive episodes (MAP < 60 mm Hg) were noted in 1, 2, and 5 patients in the remifentanil 4-, 8-, and 16-ng/mL groups, respectively. We conclude that the addition of remifentanil to propofol affects BIS only when a painful stimulus is applied. Moreover, remifentanil attenuated or abolished increases in BIS and MAP after tracheal intubation in a comparable dose-dependent fashion. IMPLICATIONS: Bispectral index change is as sensitive as hemodynamic responses after a painful stimulus for detecting deficits in the analgesic component of anesthesia. It may, therefore, be a useful monitor of the depth of anesthesia in patients who are incapable of HR and MAP responses to noxious stimuli because of medications or cardiovascular disease.     

Propofol vs. thiopental-isoflurane for neurosurgical anesthesia: comparison of hemodynamics, CSF pressure, and recovery

Sixty otherwise healthy patients with no clinical signs of intracranial hypertension who were undergoing elective intracranial surgery were randomly assigned to receive anesthesia with either thiopental, 3-6 mg/kg i.v., and isoflurane, 0.5-1.5% (group 1, N = 30) or propofol, 1-2.5 mg/kg i.v., and propofol infusion, 40-200 microg/kg/h (group 2, N = 30). Both groups received 50% nitrous oxide in O2 subsequent to dural opening. During induction, the changes in heart rate (HR), mean arterial pressure (MAP), cerebrospinal fluid pressure (CSFP), and cerebral perfusion pressure (CPP) were similar between the groups, except at 3 min when the findings (mean +/- SEM) for CPP (81 +/- 3.3 vs. 70.3 +/- 2.8 mm Hg, p <0.05) were significantly lower in group 2. At intubation, the highest level of MAP (103.1 +/- 3.3 vs. 88.9 +/- 2.7 mm Hg, p <0.05) was significantly greater in group 1. At pinhead-holder application, the highest values of HR (81.8 +/- 3 vs. 73.9 +/- 2.1 beats/min, p <0.05), MAP (112.2 +/- 3.6 vs. 98.3 +/- 3 mm Hg, p <0.05), CSFP (15.2 +/- 1.3 vs. 11.6 +/- 1.1 mm Hg, p <0.05), and CPP (97.0 +/- 3.9 vs. 86.7 +/- 3.3 mm Hg, p <0.05) were significantly greater in group 1. During early (20-30 min) recovery, group 2 had higher Glasgow Coma Scale scores and a greater percentage of patients in whom eye opening, response to commands, extubation, speech, and time/space orientation were present. In conclusion, when compared to thiopentalisoflurane for intracranial surgery, propofol produces similar HR, MAP, CSFP, and CPP responses during induction, adequate control of these responses during nociceptive stimulation, and faster recovery for cerebral function postoperatively.     

Anesthetic modification of hemodynamic and neuroendocrine stress responses to cesarean delivery in women with severe preeclampsia.

We conducted a prospective evaluation of the comparative effects of lumbar epidural and general anesthesia on the hemodynamic and neuroendocrine stress response to cesarean delivery in 21 women with severe preeclampsia. In the epidural group (n = 11), anesthesia extending to the T-4 dermatome level was obtained using 2% plain lidocaine in divided doses. In the general anesthesia group (n = 10), anesthesia was induced after pretreatment with labetalol or nitroglycerin. In the epidural group, mean arterial pressure (MAP) gradually decreased from 133.3 +/- 5.6 mm Hg to 119 +/- 4.4 mm Hg (P less than 0.002). After pretreatment with labetalol or nitroglycerin, MAP in the general group decreased from 131.5 +/- 4.9 mm Hg to 112.2 +/- 3.5 mm Hg (P less than 0.001). At skin incision (after tracheal intubation), MAP increased from 112.2 +/- 3.5 mm Hg to 143 +/- 5.4 mm Hg (P less than 0.001); however, this was not significantly different from baseline MAP. In the epidural group, there were no further changes in MAP. The difference in MAP at skin incision and postpartum period between the two groups was significant (P less than 0.004 and P less than 0.009, respectively). In the general anesthesia group, both adrenocorticotropic hormone and beta-endorphin-like immunoactivity increased significantly from base levels at skin incision. The catecholamines also increased significantly and remained so throughout the study period. In the epidural group, the concentrations of these hormones decreased or remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative effects of propofol, landiolol, and nicardipine on hemodynamic and bispectral index responses to endotracheal intubation: a prospective, randomized, double-blinded study

STUDY OBJECTIVES: To examine the comparative effects of propofol, landiolol, and nicardipine on hemodynamic responses and bispectral index (BIS) changes to endotracheal intubation. SETTING: Operating room of a university-affiliated general hospital. PATIENTS: 27 ASA physical status I and II patients who were scheduled to undergo elective general surgical, urological, or gynecological procedures with general anesthesia. STUDY DESIGN: Prospective, randomized, double-blinded study. INTERVENTIONS: Patients were divided into three groups as follows: Group 1 received propofol, 1 mg/kg; Group 2 received landiolol, 0.1 mg/kg; and Group 3 received nicardipine, 1 mg. After baseline measurements were recorded, anesthesia was induced with propofol, fentanyl, and vecuronium. Patients' lungs were ventilated with 100% oxygen for 120 seconds, at which time one of one of the study drugs was administered. Laryngoscopy and tracheal intubation were performed 4 minutes after anesthetic induction. MEASUREMENTS: Cardiac index (CI) and stroke volume index (SVI) were monitored continuously. Bispectral index was also monitored continuously from 5 minutes after tracheal intubation. MAIN RESULTS: Heart rate values in Group 3 increased 30 seconds after intubation; this increase lasted for 1 minute after intubation. Systolic blood pressure in all three groups decreased after induction of anesthesia and before tracheal intubation, and values returned closer to baseline values 30 seconds after intubation. In the propofol group, CI and SVI decreased after administration of additional propofol, lasting for 30 seconds after intubation. The BIS values rapidly decreased after induction of anesthesia, with no intergroup differences noted in BIS values (propofol group, 39+/-7; landiolol group, 44+/-14; nicardipine group, 41+/-9). However, BIS was significantly lower in the propofol group than in the other two groups from 30 seconds to 5 minutes after intubation. CONCLUSIONS: Landiolol, 0.1 mg/kg, before intubation provides effective hemodynamic stability in the postintubation period.     

Effects of target concentration infusion of propofol and tracheal intubation on QTc interval

This study was designed to evaluate the effect of target controlled infusion of propofol on QTc interval and tracheal intubation. Twenty-five unpremedicated, ASA class I or II patients were selected and target concentration infusion of propofol at 5 microg x ml(-1) was used throughout the study. The QTc interval was measured before anaesthetic induction (baseline, T1), 10 min after propofol infusion (T2), immediately after tracheal intubation (T3), and 1 min after tracheal intubation (T4). The QTc interval increased significantly at 10 min after the propofol infusion started compared to baseline (p = 0.003). After tracheal intubation, the QTc interval was further increased when compared to that at T2 (p < 0.0001). The increased QTc interval was within normal limit and no patient had an arrhythmia. In conclusion, although statistically significant, the increase in QTc interval was too small to be clinically significant during propofol infusion. However, the combination of propofol and tracheal intubation must be used carefully in patients with prolonged QTc interval.     

右美托咪啶预防全麻气管插管和拔管心血管反应的临床观察

目的 观察右美托咪啶预防全身麻醉气管插管和拔管过程中心血管反应的临床效果。方法 选择30例拟在全身麻醉下行择期腹部手术的患者（ASAⅠ～Ⅱ级）,随机分为2组：对照组（C组）和右美托咪啶组（D组）,每组15例。D组全麻诱导前静脉泵注右美托咪啶1ug/kg,15min泵注完;C组则静脉泵注等量的生理盐水。两组诱导用药均为丙泊酚1.5mg/kg,芬太尼3μg/kg及顺式阿曲库铵0.2mg/kg。记录并比较下列各时间点两组患者的平均动脉压（MAP）、心率（HR）、心率收缩压乘积（RPP）的变化：①注药前（基础值）,DEX或生理盐水输注后5、10、15min;②插管前1min,插管即刻,插管后1、3、5min;③拔管前5min,拔管即刻,拔管后3、5、10min。记录两组插管和拔管期间RPP＞12000的发生情况。结果 D组注药后10、15、插管前1min的HR较基础值下降（P＜0.05）。D组插管即刻、插管后1min、拔管时的MAP和HR均明显低于C组（P＜0.05）。注药后15min至拔管后各时间点D组患者的RPP均低于C组（P＜0.05）。D组在插管和拔管期间RPP＞12000的发生率明显小于C组（P＜0.05）。两组患者的苏醒时间、拔管时间和Ramsay评分比较差异无统计学意义。结论 右美托咪啶能显著减轻气管插管和拔管时的心血管反应,维持血流动力学的稳定,同时对麻醉恢复期没有影响。     

瑞芬太尼复合异丙酚麻醉诱导对气管插管条件及血流动力学的影响

目的对比不使用肌松剂的情况下,瑞芬太尼或芬太尼复合异丙酚麻醉诱导后对气管插管条件及血流动力学的影响。方法60名病人分为2组,诱导后2rain行气管插管术。分别记录诱导前、诱导后lmin及插管后2min的平均动脉压（MAP）和心率（Ha）。插管条件由操作者给予评分。结果两组插管成功率均为100％。瑞芬太尼组插管条件满意率80％,芬太尼73％。两组诱导后MAP和HR值较基础值均下降（P〈0．05）。插管后两组间的MAP值差异有统计学意义（P（0．05）。结论瑞芬太尼复合异丙酚麻醉诱导取得了同芬太尼复合异丙酚麻醉诱导一样良好的插管条件,在抑制插管引起的心血管反应方面瑞芬太尼组优于芬太尼组。