Insulin reverses bupivacaine-induced cardiac depression in dogs

We tested the hypothesis that an insulin infusion would effectively treat bupivacaine-induced cardiac depression in dogs. In 24 mongrel dogs anesthetized with pentobarbital (5 mgkg(-1)h(-1), IV), 0.5% bupivacaine was administrated at a rate of 0.5 mgkg(-1)min(-1) until the mixed venous oxygen saturation decreased to 60% or less. The bupivacaine infusion induced a decrease in mean arterial pressure, cardiac output, and heart rate. The dogs were randomly assigned to one of four groups after the end of bupivacaine infusion. The Control (C, n = 6) and Glucose (G, n = 6) groups received an IV infusion of normal saline (2 mL/kg) and glucose (2 mL/kg of 50% dextrose in water) for 15 min, respectively. The Insulin-Glucose (IG, n = 6) group received an IV bolus of regular insulin (1 U/kg), plus a glucose infusion (2 mL/kg of 50% dextrose in water) for 15 min. The Insulin-Glucose-Potassium (IGK, n = 6) group received the same dose of insulin and glucose as the IG group, plus potassium (1-3 mEqkg(-1)h(-1)). Mean arterial pressure, cardiac output, heart rate, and mixed venous oxygen saturation recovered toward baseline level more rapidly in the IG and IGK groups than in the C group (within 5 min versus more than 20 min). These results suggest that the infusion of insulin and glucose might reverse bupivacaine-induced cardiac depression in dogs. Implications: We found that insulin and glucose rapidly reversed hemodynamic abnormality in dogs with bupivacaine-induced cardiac depression. This study implies a possible clinical application of insulin treatment for bupivacaine-induced cardiac depression.     

Resuscitation strategies from bupivacaine-induced cardiac arrest

Objectives: Local anesthetic (LA) intoxication with cardiovascular arrest is a potential fatal complication of regional anesthesia. Lipid resuscitation has been recommended for the treatment of LA‐induced cardiac arrest. Aim of the study was to compare four different rescue regimens using epinephrine and/or lipid emulsion and vasopressin to treat cardiac arrest caused by bupivacaine intoxication. Methods: Twenty‐eight piglets were randomized into four groups (4 × 7), anesthetized with sevoflurane, intubated, and ventilated. Bupivacaine was infused with a syringe driver via central venous catheter at a rate of 1 mg·kg^?1·min^?1 until circulatory arrest. Bupivacaine infusion and sevoflurane were then stopped, chest compression was started, and the pigs were ventilated with 100% oxygen. After 1 min, epinephrine 10 μg·kg^?1 (group 1), Intralipid^® 20% 4 ml·kg^?1 (group 2), epinephrine 10 μg·kg^?1 + Intralipid^® 4 ml·kg^?1 (group 3) or 2 IU vasopressin + Intralipid^® 4 ml·kg^?1 (group 4) were administered. Secondary epinephrine doses were given after 5 min if required. Results: Survival was 71%, 29%, 86%, and 57% in groups 1, 2, 3, and 4. Return of spontaneous circulation was regained only by initial administration of epinephrine alone or in combination with Intralipid^®. Piglets receiving the combination therapy survived without further epinephrine support. In contrast, in groups 2 and 4, return of spontaneous circulation was only achieved after secondary epinephrine rescue. Conclusions: In cardiac arrest caused by bupivacaine intoxication, first‐line rescue with epinephrine and epinephrine + Intralipid^® was more effective with regard to survival than Intralipid^® alone and vasopressin + Intralipid^® in this pig model.     

Insulin/glucose infusion successfully resuscitates bupivacaine-induced sudden-onset circulatory collapse in dogs

Purpose

In previous studies, insulin reversed the cardiac toxicity gradually induced by a continuous infusion of bupivacaine. In this randomized controlled study, we intended to simulate a more relevant clinical situation by injecting bupivacaine rapidly as a bolus to induce sudden-onset circulatory collapse in dogs. We then evaluated the insulin effect.

Methods

Bupivacaine (10 mg·kg^?1 iv) was rapidly administered intravenously to 12 dogs. At the onset of circulatory collapse (defined as a mean arterial pressure [MAP] of 30 mmHg), external chest compression was initiated. Insulin (2 U·kg^?1 iv) was given to the insulin-glucose (IG) group (n = 6) and the same volume of 0.9% saline was given to the control (C) group (n = 6). The primary outcome was successful resuscitation defined as both MAP ≥ 60 mmHg and sinus rhythm on an electrocardiogram that lasted ≥ 60 sec. Hemodynamic and blood variables were measured, including cardiac output and electrocardiogram intervals.

Results

All IG dogs were successfully resuscitated within 15 (3) min, whereas none of the control dogs were resuscitated (P = 0.002). After circulatory collapse, the average MAP was higher in group IG than in group C (P = 0.006).

Conclusion

Insulin effectively reversed the sudden-onset circulatory collapse in dogs caused by an intravenous bolus injection of bupivacaine.     

脂肪乳剂复合肾上腺素对布比卡因诱发兔心脏停搏的复苏效果

目的 评价脂肪乳剂复合肾上腺素对布比卡因诱发兔心脏停搏的复苏效果.方法 雄性新西兰大白兔24只,体重2.0～2.5 kg,随机分为4组(n=6),麻醉下行气管插管,开胸暴露心脏,麻醉给药后60 min,经耳缘静脉注射布比卡因10 mg/kg,心跳停搏后行胸内心脏按压,限定按压时限30 min,同时Ⅰ组静脉输注乳酸钠林格氏液8 ml/ks 10 min;Ⅱ组静脉输注长链脂肪乳剂8 ml/kg 10 min;Ⅲ组静脉输注乳酸钠林格氏液8 ml/ks 10 min,同时静脉注射0.1%肾上腺素25 μg/kg后静脉输注0.1%肾上腺素120 min,维持MAP 80～90 mm Hg;Ⅳ组静脉输注长链脂肪乳剂8 ml/kg 10 min,同时静脉注射0.1%肾上腺素25 μg/kg后静脉输注0.1%肾上腺素120 min,维持MAP 80～90mm Hg.肾上腺素极量为8μg·kg~(-1)·min~(-1).记录开始复苏后30 min内和120 min内兔生存情况,记录Ⅲ组和Ⅳ组肾上腺素用量.结果 Ⅰ组和Ⅱ组复苏全部失败.与Ⅲ组比较,Ⅳ组开始复苏后120 min内的生存率升高,生存时间延长,肾上腺素用量降低(P＜0.05或0.01).结论 脂肪乳剂不仅可有效复苏布比卡因诱发的兔心脏停搏,还可降低肾上腺素用量.     

The effect of insulin on the resuscitation of bupivacaine-induced severe cardiovascular toxicity in dogs

Resuscitation after bupivacaine-induced cardiovascular collapse is difficult and often resistant to conventional treatment. We tested the hypothesis that insulin treatment would effectively reverse bupivacaine-induced cardiovascular collapse in pentobarbital-anesthetized dogs. Bupivacaine was administered at 0.5 mg. kg(-1). min(-1) until mean arterial blood pressure decreased to 40 mm Hg or less. In the insulin-glucose-potassium (IGK) group (n = 7), an IV bolus of regular insulin (2 U/kg) was given, followed by a glucose infusion (2 mL/kg of 50% dextrose in water) for 30 min and a potassium infusion (1-2 mmol. kg(-1). h(-1)). In the control group (n = 7), glucose infusion was given as in the IGK group. In contrast to the control group, all IGK dogs survived. Mean arterial blood pressure, heart rate, cardiac output, mixed venous oxygen saturation, and end tidal CO(2) recovered toward baseline levels in the IGK group. In conclusion, severe bupivacaine-induced cardiovascular collapse in dogs was effectively reversed with the insulin treatment.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

Resuscitation from bupivacaine-induced cardiovascular toxicity during partial inferior vena cava occlusion

The hemodynamic effects and ability to resuscitate animals experiencing bupivacaine cardiovascular toxicity after partial inferior vena cava occlusion were investigated in anesthetized dogs (n = 12). Partial occlusion of the inferior vena cava resulted in a 12% decrease in mean arterial pressure, a 62% decrease in cardiac output, a 66% decrease in stroke volume, and a 135% increase in systemic vascular resistance. Bupivacaine, 20 mg/kg intravenously, resulted in cardiovascular collapse in all animals. The resuscitation time for animals without partial caval occlusion was 2.1 +/- 0.5 min, whereas that for animals with partial caval occlusion was 22.2 +/- 6.9 min (P less than 0.05). Significantly increased amounts of epinephrine and NaHCO3 were required to resuscitate the animals with caval occlusion. We conclude that partial inferior vena cava occlusion can significantly alter the ability to resuscitate animals experiencing bupivacaine cardiovascular toxicity.