Abstract：
UNASSIGNED: Ropivacaine is considered to have a wider margin of cardiovascular safety. However, several reports of ventricular arrhythmias (VA) due to ropivacaine toxicity have been documented. Intravenous lipid emulsions (ILEs) have recently been used successfully in the treatment of local anesthetic intoxication. The main objective of the present study was to evaluate the efficacy of the ILEs in the prevention of pacing-induced-VA and electrophysiological alterations in an animal model of ropivacaine toxicity.
UNASSIGNED: Nineteen pigs were anesthetized and instrumentalized. A baseline programmed electrical ventricular stimulation protocol (PEVSP) to induce VA was performed. Ropivacaine (5 mg·kg-1 + 100 μg·kg-1·min-1) followed by normal saline infusion (control group n = 8) or intralipid 20% (1.5 mL·kg-1 + 0.25 mL·kg-1·min-1) for the ILE group (n = 8), were administered three minutes after the ropivacaine bolus. PEVSP was repeated 25 min after the onset of ropivacaine infusion. Pacing-induced VA and electrophysiological abnormalities were assessed in both groups. A sham-control group (n = 3) without ropivacaine infusion was included.
UNASSIGNED: Most of the electrophysiological parameters evaluated were affected by ropivacaine: PR interval by 28% (p = 0.001), AV interval by 40% (p = 0.001), sinus QRS by 101% (p = 0.001), paced QRS at a rate of 150 bpm by 258% (p = 0.001), and at 120 bpm by 241% (p = 0.001). Seven animals (87.5%) in the control group and eight animals (100%) in the ILE group developed sustained-VA (p = 0.30). Successful resuscitation occurred in 100% of animals in the ILE group vs. 57% of animals in the control group, p = 0.038. Pacing-induced-VA terminated at the first defibrillation attempt in 75% of the animals in the ILE group vs. 0% in the control group, p = 0.01.
UNASSIGNED: Ropivacaine strongly altered the parameters of ventricular conduction, thus facilitating the induction of VA. ILEs did not prevent pacing-induced VA. However, facilitated resuscitation and termination of VA were delivered at the first defibrillation attempt compared to the control group.
UNASSIGNED: Nineteen pigs were anesthetized and instrumentalized. A baseline programmed electrical ventricular stimulation protocol (PEVSP) to induce VA was performed. Ropivacaine (5 mg·kg-1 + 100 μg·kg-1·min-1) followed by normal saline infusion (control group n = 8) or intralipid 20% (1.5 mL·kg-1 + 0.25 mL·kg-1·min-1) for the ILE group (n = 8), were administered three minutes after the ropivacaine bolus. PEVSP was repeated 25 min after the onset of ropivacaine infusion. Pacing-induced VA and electrophysiological abnormalities were assessed in both groups. A sham-control group (n = 3) without ropivacaine infusion was included.
UNASSIGNED: Most of the electrophysiological parameters evaluated were affected by ropivacaine: PR interval by 28% (p = 0.001), AV interval by 40% (p = 0.001), sinus QRS by 101% (p = 0.001), paced QRS at a rate of 150 bpm by 258% (p = 0.001), and at 120 bpm by 241% (p = 0.001). Seven animals (87.5%) in the control group and eight animals (100%) in the ILE group developed sustained-VA (p = 0.30). Successful resuscitation occurred in 100% of animals in the ILE group vs. 57% of animals in the control group, p = 0.038. Pacing-induced-VA terminated at the first defibrillation attempt in 75% of the animals in the ILE group vs. 0% in the control group, p = 0.01.
UNASSIGNED: Ropivacaine strongly altered the parameters of ventricular conduction, thus facilitating the induction of VA. ILEs did not prevent pacing-induced VA. However, facilitated resuscitation and termination of VA were delivered at the first defibrillation attempt compared to the control group.
摘要：
■罗哌卡因被认为具有更广泛的心血管安全性。然而,已经记录了一些由于罗哌卡因毒性引起的室性心律失常(VA)的报道.静脉内脂肪乳剂（ILE）最近已成功用于治疗局部麻醉药中毒。本研究的主要目的是评估ILE在罗哌卡因毒性动物模型中预防起搏诱导的VA和电生理改变的功效。
■将19头猪麻醉并仪器化。进行基线编程的心室电刺激方案(PEVSP)以诱导VA。罗哌卡因（5mg·kg-1+100μg·kg-1·min-1），然后输注生理盐水（对照组n=8）或脂质20％（1.5mL·kg-1+0.25mL·kg-1·min-1）用于ILE组（n=8），在罗哌卡因推注后三分钟给药。在罗哌卡因输注开始后25分钟重复PEVSP。在两组中评估起搏诱导的VA和电生理异常。包括未输注罗哌卡因的假对照组（n=3）。
■评估的大多数电生理参数受罗哌卡因：PR间期28％的影响（p=0.001），房室间隔40%(p=0.001)，窦QRS下降101%(p=0.001)，以150bpm的速率将QRS调定了258%(p=0.001)，在120bpm时下降241%(p=0.001)。对照组中的7只动物(87.5%)和ILE组中的8只动物(100%)发生持续的VA(p=0.30)。ILE组100％的动物成功复苏对照组中57%的动物,p=0.038。在ILE组中，有75％的动物首次尝试除颤时，起搏诱导的VA终止。对照组为0%，p=0.01。
■罗哌卡因强烈改变了心室传导参数，从而促进VA的诱导。ILE不能预防起搏诱导的VA。然而,与对照组相比,在第一次尝试除颤时实施了促进复苏和VA终止.
■将19头猪麻醉并仪器化。进行基线编程的心室电刺激方案(PEVSP)以诱导VA。罗哌卡因（5mg·kg-1+100μg·kg-1·min-1），然后输注生理盐水（对照组n=8）或脂质20％（1.5mL·kg-1+0.25mL·kg-1·min-1）用于ILE组（n=8），在罗哌卡因推注后三分钟给药。在罗哌卡因输注开始后25分钟重复PEVSP。在两组中评估起搏诱导的VA和电生理异常。包括未输注罗哌卡因的假对照组（n=3）。
■评估的大多数电生理参数受罗哌卡因：PR间期28％的影响（p=0.001），房室间隔40%(p=0.001)，窦QRS下降101%(p=0.001)，以150bpm的速率将QRS调定了258%(p=0.001)，在120bpm时下降241%(p=0.001)。对照组中的7只动物(87.5%)和ILE组中的8只动物(100%)发生持续的VA(p=0.30)。ILE组100％的动物成功复苏对照组中57%的动物,p=0.038。在ILE组中，有75％的动物首次尝试除颤时，起搏诱导的VA终止。对照组为0%，p=0.01。
■罗哌卡因强烈改变了心室传导参数，从而促进VA的诱导。ILE不能预防起搏诱导的VA。然而,与对照组相比,在第一次尝试除颤时实施了促进复苏和VA终止.
