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Use of intravenous lidocaine to treat dexmedetomidine-induced bradycardia in sedated and anesthetized dogs
Veterinary Anaesthesia and Analgesia ( IF 1.4 ) Pub Date : 2020-12-23 , DOI: 10.1016/j.vaa.2020.11.005
Tainor Tisotti 1 , Alexander Valverde 1 , Ashley Hopkins 1 , M Lynne O'Sullivan 2 , Brad Hanna 3 , Luis Arroyo 1
Affiliation  

Objective

To assess cardiopulmonary function in sedated and anesthetized dogs administered intravenous (IV) dexmedetomidine and subsequently administered IV lidocaine to treat dexmedetomidine-induced bradycardia.

Study design

Prospective, randomized, crossover experimental trial.

Animals

A total of six purpose-bred female Beagle dogs, weighing 9.1 ± 0.6 kg (mean ± standard deviation).

Methods

Dogs were randomly assigned to one of three treatments: dexmedetomidine (10 μg kg–1 IV) administered to conscious (treatments SED1 and SED2) or isoflurane-anesthetized dogs (end-tidal isoflurane concentration 1.19 ± 0.04%; treatment ISO). After 30 minutes, a lidocaine bolus (2 mg kg–1) IV was administered in treatments SED1 and ISO, followed 20 minutes later by a second bolus (2 mg kg–1) and a 30 minute lidocaine constant rate infusion (L-CRI) at 50 (SED1) or 100 μg kg–1 minute–1 (ISO). In SED2, lidocaine bolus and L-CRI (50 μg kg–1 minute–1) were administered 5 minutes after dexmedetomidine. Cardiopulmonary measurements were obtained after dexmedetomidine, after lidocaine bolus, during L-CRI and 30 minutes after discontinuing L-CRI. A mixed linear model was used for comparisons within treatments (p < 0.05).

Results

When administered after a bolus of dexmedetomidine, lidocaine bolus and L-CRI significantly increased heart rate and cardiac index, decreased mean blood pressure, systemic vascular resistance index and oxygen extraction ratio, and did not affect stroke volume index in all treatments.

Conclusion and clinical relevance

Lidocaine was an effective treatment for dexmedetomidine-induced bradycardia in healthy research dogs.



中文翻译:

静脉注射利多卡因治疗镇静和麻醉犬右美托咪定诱发的心动过缓

客观的

评估静脉注射 (IV) 右美托咪定和随后静脉注射利多卡因以治疗右美托咪定引起的心动过缓的镇静和麻醉犬的心肺功能。

学习规划

前瞻性、随机、交叉实验试验。

动物

总共六只特制雌性比格犬,重 9.1 ± 0.6 kg(平均值 ± 标准差)。

方法

狗被随机分配到三种治疗中的一种:右美托咪定(10 μg kg –1 IV)给予清醒(治疗 SED1 和 SED2)或异氟醚麻醉的狗(呼气末异氟醚浓度 1.19 ± 0.04%;治疗 ISO)。30 分钟后,在 SED1 和 ISO 治疗中给予利多卡因推注 (2 mg kg –1 ) IV,20 分钟后进行第二次推注 (2 mg kg –1 ) 和 30 分钟利多卡因恒速输注 (L-CRI) ) 50 (SED1) 或 100 μg kg –1分钟–1 (ISO)。在 SED2 中,利多卡因推注和 L-CRI(50 μg kg –1分钟–1) 在右美托咪定后 5 分钟给药。在右美托咪定后、利多卡因推注后、L-CRI 期间和停止 L-CRI 后 30 分钟获得心肺测量值。混合线性模型用于治疗内的比较(p < 0.05)。

结果

当在推注右美托咪定后给药时,利多卡因推注和 L-CRI 显着增加心率和心脏指数,降低平均血压、全身血管阻力指数和氧气提取率,并且在所有治疗中均不影响每搏输出量指数。

结论和临床相关性

利多卡因是治疗健康研究犬右美托咪定诱发的心动过缓的有效方法。

更新日期:2021-03-02
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