Effect of dexmedetomidine on haemodynamic responses to laryngoscopy and intubation : perioperative haemodynamics and anaesthetic requirements

BACKGROUND: Dexmedetomidine reduces the dose requirements for opioids and anaesthetic agents. The purpose of this study was to evaluate the effect of a single pre-induction intravenous dose of dexmedetomidine 1 microg/kg on cardiovascular response resulting from laryngoscopy and endotracheal intubation, need for anaesthetic agent and perioperative haemodynamic stability. METHODS: Fifty patients scheduled for elective minor surgery were randomised into two groups (dexmedetomidine group and placebo group, n = 25 in each group). During and after drug administration, the Ramsey sedation scale was applied every 5 minutes. Fentanyl 1 microg/kg was administered to all patients and thiopental was given until lash reflex disappeared. Anaesthesia continuation was maintained with 50% : 50%, oxygen : nitrous oxide. Sevoflurane concentration was adjusted to maintain systolic blood pressure within 20% of preoperative values. After extubation, the Steward awakening score was applied at 5 and 10 minutes. Haemodynamic parameters and adverse effects were recorded every 10 minutes for 1 hour after surgery. RESULTS: During intubation the need for thiopental and sevoflurane concentration were decreased by 39% and 92%, respectively, in the dexmedetomidine group compared with the placebo group. In all groups, blood pressure and heart rate increased after tracheal intubation; both were significantly lower in the dexmedetomidine group than in the placebo group (p < 0.05). Fentanyl requirement during the operation was 74.20 +/- 10.53microg in the dexmedetomidine group and 84.00 +/- 27.04microg in the placebo group (p < 0.05). At 5 minutes, the Steward scores were >6 in 56% of the dexmedetomidine group and in 4% of the placebo group (p < 0.05). At 10 minutes, sedation scores were > or =4 in all patients in the dexmedetomidine group (p < 0.05). Arterial blood pressure and heart rate in the postoperative period were significantly lower in the dexmedetomidine group compared with the placebo group (p < 0.05). CONCLUSION: Preoperative administration of a single dose of dexmedetomidine resulted in progressive increases in sedation, blunted the haemodynamic responses during laryngoscopy, and reduced opioid and anaesthetic requirements. Furthermore, dexmedetomidine decreased blood pressure and heart rate as well as the recovery time after the operation.     

Dexmedetomidine: a review of its use for sedation in mechanically ventilated patients in an intensive care setting and for procedural sedation

Dexmedetomidine (Precedex?), a pharmacologically active dextroisomer of medetomidine, is a selective α(2)-adrenergic receptor agonist. It is indicated in the US for the sedation of mechanically ventilated adult patients in an intensive care setting and in non-intubated adult patients prior to and/or during surgical and other procedures. This article reviews the pharmacological properties, therapeutic efficacy and tolerability of dexmedetomidine in randomized, double-blind, placebo-controlled, multicentre studies in these indications. Post-surgical patients in an intensive care setting receiving dexmedetomidine required less rescue sedation with intravenous propofol or intravenous midazolam to achieve and/or maintain optimal sedation during the assisted ventilation period than placebo recipients, according to two randomized, double-blind, multinational studies. Moreover, significantly more dexmedetomidine than placebo recipients acquired and/or maintained optimal sedation without rescue sedation. Sedation with dexmedetomidine was also effective in terms of the total dose of morphine administered, with dexmedetomidine recipients requiring less morphine than placebo recipients; with regard to patient management, dexmedetomidine recipients were calmer and easier to arouse and manage than placebo recipients. Intravenous dexmedetomidine was effective as a primary sedative in two randomized, double-blind, placebo-controlled, multicentre studies in adult patients undergoing awake fibre-optic intubation or a variety of diagnostic or surgical procedures requiring monitored anaesthesia care. In one study, significantly fewer dexmedetomidine than placebo recipients required rescue sedation with intravenous midazolam to achieve and/or maintain optimal sedation; conversely, in another study, rescue sedation with intravenous midazolam was not required by significantly more dexmedetomidine than placebo recipients. Primary sedation with intravenous dexmedetomidine was also effective in terms of the secondary efficacy endpoints, including the mean total dose of midazolam and fentanyl administered and the percentage of patients requiring further sedation (in addition to dexmedetomidine or placebo and midazolam), with, for the most part, significant between-group differences observed in favour of dexmedetomidine over placebo. In general, no significant differences were observed between the dexmedetomidine and placebo treatment groups in the anaesthesiologists' assessment of ease of intubation, haemodynamic stability, patient cooperation and/or respiratory stability. Intravenous dexmedetomidine is generally well tolerated when utilized in mechanically ventilated patients in an intensive care setting and for procedural sedation in non-intubated patients. Dexmedetomidine is associated with a lower rate of postoperative delirium than midazolam or propofol; it is not associated with respiratory depression. While dexmedetomidine is associated with hypotension and bradycardia, both usually resolve without intervention. Thus, intravenous dexmedetomidine provides a further option as a short-term (<24 hours) primary sedative in mechanically ventilated adult patients in an intensive care setting and in non-intubated adult patients prior to and/or during surgical and other procedures.     

右美托咪定对丙泊酚靶控输注意识消失半数有效浓度的影响

目的探讨右美托咪定对丙泊酚靶控输注(TCI)时患者意识消失的半数有效浓度(EC50)的影响。方法择期全身麻醉手术患者40例(ASAⅠ～Ⅱ级),随机分成两组(n=20):右美托咪定组(D组)和对照组(C组)。D组麻醉诱导前经微量泵泵注右美托咪定负荷量0.4μg/kg(15min)静脉输注完毕,然后以0.4μg/(kg·h)维持输注,C组泵注等量生理盐水。麻醉诱导采用丙泊酚TCI,设定起始血浆靶浓度为2.3μg/ml,按相邻浓度比值为1.18序贯法给药,达到设定的血浆靶浓度后进行镇静/警觉评分(OAA/S),后静脉注射舒芬太尼及顺阿曲库铵,纯氧通气3min后气管插管。记录患者静脉输注右美托咪定或生理盐水前(T0),静脉输注15min后(T1),丙泊酚血浆靶浓度达到设定靶浓度时(T2),诱导后插管前(T3),插管后1min(T4)、3min(T5)、5min(T6)各时点的BIS及其MAP、HR。计算并比较D、C组丙泊酚TCI患者意识消失的EC50。结果 D、C组丙泊酚TCI患者意识消失的EC50分别为2.94μg/ml(95%的可信区间为2.79～3.10μg/ml)和3.67μg/ml(95%的可信区间为3.44～3.90μg/ml),D组低于C组(P<0.05)。T1时D组患者BIS值低于C组(P<0.05);T4时C组HR、MAP较T0时均升高(P<0.05)而D组无变化(P>0.05);T1～T6时D组患者的HR均低于C组(P<0.05)。结论右美托咪定以负荷量0.4μg/kg继以0.4μg/(kg·h)维持静脉输注可以使患者产生明显的镇静作用,降低BIS值,减轻气管插管反应,并能使丙泊酚TCI患者意识消失的EC50降低为2.94μg/ml。     

Clinical uses of dexmedetomidine in pediatric patients

Dexmedetomidine is being used off-label as an adjunctive agent for sedation and analgesia in pediatric patients in the critical care unit and for sedation during non-invasive procedures in radiology. It also has a potential role as part of anesthesia care to prevent emergence delirium and postanesthesia shivering. Dexmedetomidine is currently approved by the US FDA for sedation only in adults undergoing mechanical ventilation for <24 hours. Pediatric experiences in the literature are in the form of small studies and case reports. In patients sedated for mechanical ventilation and/or opioid/benzodiazepine withdrawal, the loading dose ranged from 0.5 to 1 microg/kg and was usually administered over 10 minutes, although not all patients received loading doses. This patient group also received a continuous infusion at rates ranging from 0.2 to 2 microg/kg/h, with higher rates used in burn patients and those with withdrawal following > or =24 hours of opioid/benzodiazepine infusion. The dexmedetomidine dosage used for anesthesia and sedation during non-invasive procedures, such as radiologic studies, ranged from a loading dose of 1-2 microg/kg followed by a continuous infusion at 0.5-1.14 microg/kg/h, with most patients spontaneously breathing. For invasive procedures, such as awake craniotomy or cardiac catheterization, dosage ranged from a loading dose of 0.15 to 1 microg/kg followed by a continuous infusion at 0.1-2 microg/kg/h. Adverse hemodynamic and respiratory effects were minimal; the agent was well tolerated in most patients. The efficacy of dexmedetomidine varied depending on the clinical situation: efficacy was greatest during non-invasive procedures, such as magnetic resonance imaging (MRI), and lowest during invasive procedures, such as cardiac catheterization. Dexmedetomidine may be useful in pediatric patients for sedation in a variety of clinical situations. The literature suggests potential use of dexmedetomidine as an adjunctive agent to other sedatives during mechanical ventilation and opioid/benzodiazepine withdrawal. In addition, because of its minimal respiratory effects, dexmedetomidine has also been used as a single agent for sedation during non-invasive procedures such as MRI. However, additional studies in pediatric patients are warranted to further evaluate its safety and efficacy in all age ranges.     

右美托咪定用于机械通气患者镇静的疗效观察

目的观察右美托咪定对于机械通气患者镇静的疗效。方法将2012年ICU住院机械通气患者60例按随机、对照原则分为右美托咪定组(D)和丙泊酚组(P),分别记录两组患者用药前后Ramsay镇静评分、心率情况及用药前后血压的控制情况,对数据进行统计学分析。结果两组患者不同时间段Ramsay镇静评分、心率以及用药前后血压控制的差异具有统计学意义。结论右美托咪定的镇静效果好于丙泊酚,且血流动力学稳定。     

麻醉诱导期间靶控输注舒芬太尼对丙泊酚镇静作用的影响

目的:探讨麻醉诱导期间不同浓度舒芬太尼对睫毛反射、意识消失时丙泊酚血药浓度的影响。方法:选择40例择期手术患者靶控输注舒芬太尼、丙泊酚全凭静脉麻醉,根据舒芬太尼目标浓度将患者分为4组,分别为0ng·mL-(1A组)、0.2ng·mL-(1B组)、0.4ng·mL-(1C组)、0.8ng·mL-(1D组),每组10例。应用高效液相色谱-质谱联用法测定舒芬太尼血药浓度,反相高效液相色谱法测定丙泊酚血药浓度。结果:麻醉诱导睫毛反射与意识消失时,单用丙泊酚血药浓度分别为2.74μg·mL-1、3.87μg·mL-1;舒芬太尼靶浓度从0.2ng·mL-1升至0.8ng·mL-1,睫毛反射消失时丙泊酚血药浓度从2.67μg·mL-1降至1.58μg·mL-1、意识消失时从3.90μg·mL-1降至2.61μg·mL-1;舒芬太尼与丙泊酚在睫毛反射、意识消失时的量效关系均呈直线关系;D组分别与A、B组比较,在睫毛反射与意识消失时丙泊酚的效应室浓度均明显减少(P<0.05);D组与C组比较,在睫毛反射消失时丙泊酚的效应室浓度也明显减少。结论:麻醉诱导期舒芬太尼与丙泊酚在镇静催眠作用方面表现为相加作用,舒芬太尼靶浓度0.4～0.8ng·mL-1时可明显降低丙泊酚在睫毛反射与意识消失时的血药浓度,推荐临床应用舒芬太尼靶浓度0.4～0.8ng·mL-1为宜。     

Dexmedetomidine

Dexmedetomidine is a potent alpha2-adrenoceptor agonist with 8 times higher affinity for the alpha2-adrenoceptor than clonidine. Dexmedetomidine has shown sedative, analgesic and anxiolytic effects after intravenous administration to healthy volunteers or postsurgical patients in the intensive care unit. Dexmedetomidine produced a predictable haemodynamic decline (dose-dependently decreased arterial blood pressure and heart rate) in postsurgical patients coinciding with reductions in plasma catecholamines. In phase III clinical trials, dexmedetomidine 0.2 to 0.7 microg/kg/h produced clinically effective sedation and significantly reduced the analgesic requirements of postsurgical ventilated intensive care unit patients. There was no clinically apparent respiratory depression after cessation of assisted ventilation. Dexmedetomidine produced rapid and stable sedation in postsurgical ventilated patients while maintaining a high degree of patient rousability and anxiety reduction. Dexmedetomidine was well tolerated in phase III studies. The most frequently observed adverse events were hypotension, bradycardia and nausea.     

Severe Rash Associated with Dexmedetomidine Use During Mechanical Ventilation

Dexmedetomidine, a sedative administered by continuous infusion, is used to facilitate mechanical ventilation through α₂-receptor activation. The drug's most common adverse reactions include hypotension, hypertension, nausea, bradycardia, and dry mouth. However, to our knowledge, no reports of dermatologic allergic reactions from dexmedetomidine use have been published. We describe a 22-year-old man who was intubated after being injured in a motor vehicle collision. He had been receiving propofol and fentanyl infusions for sedation during mechanical ventilation and was transitioning to dexmedetomidine. Within 4 hours of receiving dexmedetomidine 0.2 μg/kg/hour, the patient developed a wheal-and-flare rash encompassing 60% of his body surface area. The infusion was immediately discontinued; over the next 24 hours most of the rash receded, and within 48 hours of drug discontinuation the rash had completely resolved. According to the Naranjo adverse drug reaction probability scale, the likelihood that this rash was induced by dexmedetomidine was probable. Clinicians should be aware of this potential dermatologic adverse effect from dexmedetomidine, and patients receiving the drug should be closely monitored.     

Sedation and analgesia in the intensive care unit: evaluating the role of dexmedetomidine.

PURPOSE: A review highlighting the application of sedatives and analgesics in the intensive care unit (ICU) setting, with a focus on the use of dexmedetomidine, is presented. SUMMARY: Relevant and applicable clinical trials that resulted from a search of the literature from 1966 to July 2006 using key search terms such as dexmedetomidine, intensive care unit, sedation, delirium, and analgesia were evaluated. Many agents have been evaluated in the search of the optimal regimen for sedation and analgesia in the ICU, including opioids, benzodiazepines, propofol, and antipsychotic agents. Dexmedetomidine has demonstrated efficacy as a sedative analgesic on the basis of its ability to lower opioid, benzodiazepine, and propofol requirements in clinical trials. The role of dexmedetomidine in ICU clinical practice is limited because of a lack of mortality and other morbidity endpoints, such as ICU length of stay, hospital length of stay, time to extubation, long-term complications after discharge from the ICU, and delirium. The most commonly reported adverse effects of dexmedetomidine are secondary to its effects as an alpha(2)-receptor agonist and are cardiac in nature. A detailed cost analysis may be warranted to justify the relatively high acquisition cost of dexmedetomidine. CONCLUSION: Dexmedetomidine may be an effective agent for ICU sedation and analgesia. However, the lack of clinically relevant endpoints in trials, the concern about adverse cardiovascular effects, and the relatively high acquisition cost of this drug limit its use to a select number of patients who may benefit from its distinguished mechanism of action.     

Computer-Assisted Continuous Infusion for the Delivery of Target-Controlled Infusions of Propofol During Outpatient Surgery

Propofol was administered intravenously using a first-order, three-compartment, computer-controlled infusion pump (CCIP) based on the Ohmeda 9000 syringe pump. The CCIP system produced a target-controlled infusion (TCI) based on the estimated blood concentration (EBC). Twenty-five patients undergoing ambulatory surgery completed the study. The induction EBC was 4.72 ± 0.28 μg/ml, and was achieved rapidly with minimal hemodynamic changes. The emergence EBC was 1.55 ± 0.21 μg/ml, and the discharge EBC was 1.06 ± 0.22 μg/ml. The EBC, together with clinical signs, allowed for predictable inductance and emergence from anesthesia using propofol.     

右美托咪定辅助异丙酚在腰硬联合麻醉中的镇静作用比较

目的探讨右美托咪定在联合异丙酚用于腰-硬联合麻醉的镇静效果。方法 150例妇产科需要手术患者,随机分为A、B、C三组,每组各50例,分别给予不同药物,分析比较三组患者给药前后中心静脉压及心率的变化。结果三组给药后2min中心静脉压及心率明显下降,且A组比B、C两组的中心静脉压、心率有明显下降;A、B两组相比,A组中心静脉压和心率也明显下降。同时发现:手术中异丙酚得使用量A组最少,三组比较均有统计学差异(P<0.05)。结论右美托咪定联合异丙酚在妇产科手术腰-硬联合麻醉中发挥了良好的镇静作用,并可有效的减少异丙酚用量,不良反应少。     

右美托咪定辅助全身麻醉患者的镇静及全身麻醉药物的节俭作用

目的探讨右美托咪定辅助全身麻醉患者的镇静及全身麻醉药物的节俭作用。方法对本院2012年2月～2013年1月收治的全身麻醉患者的临床治疗病例进行抽样,将40例全身麻醉患者按照抽签法随机分为对照组与观察组,每组各20例。对照组采用氯化钠注射液静脉注射治疗,然后使用丙泊酚进行全身麻醉诱导,观察组采用右美托咪定注射液静脉注射治疗。结果两组全身麻醉患者经过镇静治疗后的镇静效果及全身麻醉药物的使用情况差异有统计学意义（P〈0．05）。结论全身麻醉患者采用右美托咪定辅助全身麻醉的镇静及全身麻醉药物的使用量明显低于传统镇静治疗药物的使用情况,具有显著的节俭作用,能够有效缓解全身麻醉患者的痛苦。值得临床推广应用。     

右美托咪啶用于ICU颅脑病变患者的镇静

目的研究右美托咪啶用于ICU颅脑病变患者的镇静作用。方法对50例颅脑病变患者给予右美托咪啶镇静,维持Ramsay评分2～5分,观察各项指标。结果镇静效率为（86.6±7.3）%,镇静时间平均输注速度为（0.52＋0.13）μg/（kg·h）,镇静生命体征平稳。结论右美托咪啶可有效应用于颅脑病变患者,且具有独特优势。     

右美托咪定复合丙泊酚在无痛肠镜检查中的应用

目的：观察右美托咪定复合丙泊酚用于无痛肠镜检查的临床效果及安全性。方法：选择用肠镜检查患者66例,随机分成二组P组（n＝33）、D组（n＝33）,入室开放上肢静脉,吸氧,监测血压、心率、血氧饱和度,D组先0.1μg/kg/min静脉推注右美托咪定（0.1μg/kg）,P组静脉推注安慰剂（0.9%生理盐水）3ml后,再2 mg/kg/min静脉推注丙泊酚（1.5 mg/kg）,完成后待睫毛反射消失,开始插镜,检查中如有体动反应,追加丙泊酚30～50mg,并观察丙泊酚用量,及体动,循环、呼吸抑制等副作用。结果：丙泊酚总用药量,可唤醒时间P组明显高于D组,差异有统计学意义（ p〈0.05）;D组体动发生例数明显低于P组,差异有统计学意义（p〈0.05）;用丙泊酚实施无痛麻醉过程中均可导致循环抑制,心率加快,右美托咪定对循环影响小,能导致心率降低,可拮抗丙泊酚的心率加快作用,差异有统计学意义p〈0.05。结论：小剂量右美托咪定在无痛肠镜中的使用,方法简单,具有良好的安全性; 能协同丙泊酚的麻醉镇静作用,提供更佳的术中镇静效果。     

Synergy between intrathecal omega-conotoxin CVID and dexmedetomidine to attenuate mechanical hypersensitivity in the rat

The analgesic effects of intrathecal (i.t.) omega-conotoxin CVID, an N-type Ca2+ channel antagonist, and the alpha2-adrenoceptor agonist, dexmedetomidine, were tested alone and in combination following unilateral ligation of L (lumbar) 5/6 spinal nerves in rats. Mechanical allodynia was observed prior to insertion of an i.t. catheter. Effects and interactions of omega-conotoxin CVID (0.01-10 microg/kg) and dexmedetomidine (0.1-10 microg/kg) were tested on allodynic and tail flick (thermal stimulus) responses. Only dexmedetomidine increased the latency of the tail flick response. Both dexmedetomidine and omega-conotoxin CVID completely inhibited allodynia (ED50 0.78+/-0.02 and 0.35+/-0.08 microg/kg, respectively; n=63, 41). Dexmedetomidine and omega-conotoxin CVID combined in dose ratios 0.7 and 1.3 (adjusted for ED50) were synergistic in decreasing mechanical hypersensitivity; interaction index (gamma) 0.39 (confidence interval [CI] 0.33, 0.46) and 0.3 (CI 0.23, 0.38). Despite the necessity for i.t. administration, these data suggest that the synergistic combination confers enhanced potency (lower doses) of both drugs that may avoid clinical toxicity of single drug therapy.     

Rapid reversal of alpha 2-adrenoceptor agonist effects by atipamezole in human volunteers.

1. The ability of atipamezole, a specific and selective alpha 2-adrenoceptor antagonist, to reverse the pharmacological effects induced by the alpha 2-adrenoceptor agonist dexmedetomidine was studied in six healthy male volunteers. Each volunteer received in four sessions in a randomized and single-blind manner three different doses (6.7 micrograms kg-1, 27 micrograms kg-1 and 67 micrograms kg-1) of atipamezole or saline placebo as 5 min i.v. infusions preceded by a fixed i.v. dose of dexmedetomidine (0.67 micrograms kg-1). 2. Dexmedetomidine caused profound sedation, with the subjects actually falling asleep. This was effectively reversed by the two highest doses of antipamezole. 3. Dexmedetomidine reduced salivary flow on average by 70%. A rapid and full reversal of this effect was seen after the highest dose of antipamezole. 4. Hypotension induced by dexmedetomidine was also effectively antagonized by atipamezole. Bradycardia was very modest after dexmedetomidine in this study, and thus no reversal of alpha 2-adrenoceptor agonist-induced bradycardia could be demonstrated. 5. Plasma noradrenaline concentrations were reduced by 80% by dexmedetomidine. This was effectively antagonized by atipamezole, and the highest dose caused a 50% overshoot in plasma noradrenaline concentrations over the basal levels. 6. It is concluded that the effects of dexmedetomidine are effectively reversible by atipamezole. A dose ratio of 10:1 for atipamezole:dexmedetomidine was clearly insufficient for this purpose, but ratios in the range of 40:1 to 100:1 were found to be effective in the current experimental situation.     

盐酸右美托咪定镇静及镇痛效果观察

目的 观察盐酸右美托咪啶在臂丛神经及椎管内阻滞麻醉中的镇静及镇痛效果.方法 选择美国麻醉医师协会（ASA）分级Ⅰ或Ⅱ级、术前未使用任何镇静及镇痛药物的臂丛神经及椎管内阻滞麻醉患者100例,随机分为盐酸右美托咪定组（观察组）和度氟合剂（哌替啶50 mg、氟哌啶醇5 mg）组（对照组）,各50例.待臂丛神经或椎管内阻滞麻醉完善、镇痛完全后,观察组予右美托咪定1.0 μg/kg,10 min静脉滴注完毕;对照组予度氟合剂半剂（5 mL）,5 min静脉缓注,分别测定用药前,用药后10、30、60 min两组患者脑干听觉诱发电位指数（AAI）、平均动脉压、心率及用药前和用药后30 min血皮质醇含量.结果 两组患者用药后AAI、平均动脉压、心率及血皮质醇含量均较用药前降低（P〈0.05）.结论 盐酸右美托咪啶在剂量选择适宜的条件下（1.0 μg/kg）与度氟合剂（半剂量）的镇静及镇痛效果相同或相似.建议在正确掌握适应证并充分考虑患者经济承受力的情况下可使用盐酸右美托咪啶.     

右美托咪啶用于重症监护病房镇静的效果评价

目的观察右美托咪啶用于重症监护病房（ICU）镇静的效果及安全性。方法选择全身麻醉腹部手术后带气管插管转入ICU患者40例,随机分为右美托咪啶组（D组）和丙泊酚组（P组）各20例。D组予右美托咪啶负荷量1μg／kg20min内静脉泵入,每1h依据Ramsay评分调整药物泵入剂量为0．2～0．7μg／（kg·h）;P组予丙泊酚负荷剂量lmg／kg静脉注射,根据不同镇静程度维持剂量为O．5～3mg／（kg·h）。每2h进行数字疼痛评分（NRS）,当NRS评分大于4分时给予芬太尼1μg／kg;达到拔管备件者拔出气管导管。结果与P组比较,D组镇静效率明显较高（P〈0．05）,芬太尼用量明显减少（P〈0．05）,停药后苏醒、拔管时间明显缩短（P〈0．05）;用药期间两组心血管事件发生率有显著性差异（P〈0．05）,术后谵妄发生率无显著性差异（P〉0．05）。结论右美托咪啶用于ICU的镇静、镇痛效果好,苏醒快,可缩短拔管时间,血流动力学稳定,谵妄发生率低,是ICU理想的镇静剂。     

咪达唑仑或丙泊酚联用右美托咪啶对颅脑创伤患者镇静作用的比较

目的:比较右美托咪啶联用丙泊酚或咪达唑仑对急性中度颅脑损伤患者镇静的临床疗效及24 h费用。方法:对75例颅脑外伤患者分别给予丙泊酚或咪达唑仑镇静,同时联合使用右美托咪啶镇静,维持镇静躁动评分(SAS)2~4分为标准,观察24 h镇静效率、生命体征、格拉斯哥昏迷程度评分(GCS)的变化,并比较两组镇静药物的总体费用。结果:右美托咪啶联用丙泊酚或咪达唑仑均能使患者达到预定的镇静镇痛目标评分,2组患者镇静前后的平均动脉压(MAP)、心率(HR)、呼吸频率(R)均有明显下降,且丙泊酚组下降幅度更明显(P<0.05);而镇静前后的血氧饱和度(SPO₂)、动脉血二氧化碳分压(PaCO₂)、GCS评分以及中心静脉压(CVP)均无明显差异(P>0.05);但联用丙泊酚组总体费用较高(558±218 比422±120,P<0.05)。结论:2组患者均可取得较好的镇静效果,但丙泊酚较咪达唑仑具有更显著的呼吸、循环抑制效应;在镇静镇痛费用方面,丙泊酚组明显高于咪达唑仑组。