右美托咪定使用患者并发室上性心律失常的电生理研究
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Dexmedetomidine use in patients undergoing electrophysiological study for supraventricular tachyarrhythmias
背景与目的
右美托咪定是一种具有镇静、镇痛、抗焦虑特性的选择性α-2肾上腺素受体激动剂，尚未被批准用于小儿。据报道，右美托咪定可降低小儿窦房结及房室结功能；已有建议表明研究右美托咪定电生理可能并不可取。我们假设在电生理研究中右美托咪定不抑制诱导的室上性心动过速(SVT)并且不抑制这种心律失常的消融。
方 法
在这项回顾性、观察性队列研究中，我们回顾了心脏导管室自2007年以来经诊断或治疗的所有SVT患者。所有病例均由同一位电生理专家施行，麻醉是由三位心脏麻醉医生中的某一位施行。其中一位心脏麻醉医生的电生理研究过程中没有使用右美托咪定；第二位应用右美托咪定，但只持续输注；第三位采用右美托咪定负荷量给药后再持续输注的方式。因此，患者被分为三个不同的组：组1未接受任何右美托咪定；组2以0.5 μg-1·kg-1 ·h-1持续输注右美托咪定；组3以0.5μg-1·kg-1负荷量，0.5 μg-1·kg-1 ·h-1输注右美托咪定。然后我们对这些患者以下变量进行比较：人口数据，包括年龄、性别、身高、体重；麻醉数据如，面罩与静脉诱导，诱导剂的组成，七氟醚和异丙酚用量；右美托咪定用量；存在的先天性心脏病和其他疾病；对异丙肾上腺素的需求及剂量，对腺苷的需求及剂量；和其他对射频消融前后节律有影响的药物；诱发心律失常的能力，心律失常的类型，沃-帕-怀综合征的存在，旁路的存在，消融率和复发率。
结 果
除了右美托咪定组异丙酚使用量较小外(χ2(2) = 48.2, P < 0.001)，麻醉药物无明显差异；各组间电生理参数无差异，除了组1患者与右美托咪定组相比，在消融前期对异丙肾上腺素确实不经常使用(χ2(2) = 15.2, P < 0.01)。然而，随着异丙肾上腺素的大量使用，诱导心律失常的能力没有差别。此外，消融患者的百分比和组间复发率相同。
结 论
我们得出这样的结论：右美托咪定不妨碍SVT的电生理研究和这种心律失常消融的成功。然而，应用右美托咪定后在需要更多的异丙肾上腺素。
原始文献摘要
Paediatr Anaesth. 2017 Jan;27(1):45-51. doi: 10.1111/pan.13019. Epub 2016 Oct 25.Tirotta CF1, Nguyen T2, Fishberger S2
BACKGROUND:
Dexmedetomidine is a selective alpha-2 adrenergic agonist with sedative, analgesic, and anxiolytic properties. Dexmedetomidine has not been approved for use in pediatrics. Dexmedetomidine has been reported to depress sinus node and atrioventricular nodal function in pediatric patients; it has been suggested that the use of dexmedetomidine may not be desirable during electrophysiological studies.AIM:We hypothesize that the use of dexmedetomidine does not inhibit the induction of supraventricular tachyarrhythmias (SVT) during electrophysiological studies and does not inhibit the ablation of such arrhythmias.
METHODS:
In this retrospective, observational cohort study, we reviewed all cases presenting to the cardiac catheterization laboratory for diagnosis or treatment of SVT since 2007. All cases were performed by the same electrophysiologist. The anesthesia was provided by one of the three cardiac anesthesiologists. One cardiac anesthesiologist did not use dexmedetomidine during electrophysiological studies. A second used dexmedetomidine, but only with an infusion. The third used dexmedetomidine with a primary bolus and an infusion. Thus, the patients were stratified into three different groups: Group 1 patients did not receive any dexmedetomidine. Group 2 patients received a dexmedetomidine infusion of 0.5-1 μg·kg-1 ·h-1 . Group 3 patients received a dexmedetomidine infusion of 0.5-1 μg·kg-1 ·h-1 and a dexmedetomidine bolus prior to the infusion of 0.5-1 μg·kg-1 . We then compared those patients for the following variables: demographic data including age, sex, height, weight; anesthetic data such as, mask vs intravenous induction, identity of induction agent, amount of sevoflurane and propofol used; amount of dexmedetomidine used; presence of congenital heart disease and other comorbidities; the need for isoproterenol and dose, the need for adenosine and dose, and the need for any other medications to affect rhythm both before and after radiofrequency ablation; the ability to induce the arrhythmia, the type of arrhythmia, the presence of Wolff-Parkinson-White syndrome, the presence of an accessory pathway, the ablation rate, and the recurrence rate.
RESULTS:
There was no difference in the anesthetic agents, except there was a lesser amount of propofol used in the dexmedetomidine groups (χ2(2) = 48.2, P < 0.001). There was no difference in the electrophysiological parameters among groups, except the Group 1 patients did require the use of isoproterenol in the preablation period less often compared to the dexmedetomidine groups (χ2(2) = 15.2, P < 0.01). However, with the greater use of isoproterenol, there was no difference in the ability to induce the arrhythmia. Moreover, the percentage of patients ablated, and the recurrence rate among groups was the same.
CONCLUSIONS:
We conclude that dexmedetomidine does not interfere with the conduct of electrophysiological studies for SVT and the successful ablation of such arrhythmias. However, dexmedetomidine use did result in a greater need for isoproterenol.
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