FACEM, Waikato Hospital, Emergency Department, Waikato Hospital, Pembroke St., Hamilton 3240, New Zealand.
Anesth Analg. 2010 Sep;111(3):791-6. doi: 10.1213/ANE.0b013e3181e66050. Epub 2010 Jun 14.
IV lipid emulsion has demonstrated to be effective therapy for bupivacaine-induced cardiotoxicity. However, the role of epinephrine when coadministered with lipid emulsion in toxin-induced cardiac arrest is unclear. We postulated superior resuscitation outcome in the absence of epinephrine in a rabbit model of bupivacaine-induced cardiac arrest resuscitated with IV lipid emulsion.
Twenty sedated, instrumented New Zealand White rabbits received 10 mg/kg IV bupivacaine producing asystole. Mechanical ventilation and external chest compressions were commenced at 30 seconds. At 1 minute, animals received 5 mL/kg 20% lipid emulsion in addition to 1 of 4 additional IV treatments (n = 5 all groups): 0.9% saline, 2.5 microg/kg epinephrine, 10 microg/kg epinephrine, 100 microg/kg epinephrine; all at 1 mL/kg. Lipid emulsion bolus was repeated at 4 minutes. Return of spontaneous circulation and hemodynamic metrics were obtained to 15 minutes. Saline group animals additionally received high-dose epinephrine (100 microg/kg) treatment at 15 minutes, and were monitored to 20 minutes.
High-dose epinephrine administration was associated with increased rate of return of spontaneous circulation compared with saline control (0 of 5 saline-treated animals; 0 of 5 animals in the 2.5 microg/kg epinephrine group; 3 of 5 in the 10 microg/kg group [P = 0.167]; and 4 of 5 in the 100 microg/kg group [P = 0.048]). Spontaneous but decreasing circulation was maintained at 15 minutes in 4 of 5 animals in the 100 microg/kg group alone (P = 0.048); mean arterial blood pressure at 15 minutes was 12.8 (SEM 2.8) mm Hg saline, 12.0 (2.5) mm Hg 2.5 microg/kg epinephrine, 20.6 (2.7) mm Hg 10 microg/kg epinephrine, and 26.4 (3.9) mm Hg 100 microg/kg epinephrine (P = 0.008). Four of five animals in the saline-treated group exhibited return of spontaneous circulation after delayed epinephrine treatment (P = 0.048). High-dose epinephrine administration was associated with a significant increase in coronary perfusion pressure before return of spontaneous circulation.
Epinephrine seemed to be necessary for return of spontaneous circulation, but was subsequently associated with declining hemodynamic variables in this rabbit model of bupivacaine-induced cardiac arrest. Further study is required to define the role of epinephrine in lipid-based resuscitation from local anesthetic-induced cardiac arrest.
静脉内脂肪乳剂已被证明对布比卡因引起的心脏毒性有效。然而，当与脂肪乳剂联合使用时，肾上腺素在毒素引起的心脏骤停中的作用尚不清楚。我们假设在没有肾上腺素的情况下，兔布比卡因引起的心脏骤停复苏模型中使用静脉内脂肪乳剂复苏会有更好的复苏结果。
20 只镇静、仪器化的新西兰白兔接受 10 mg/kg 静脉内布比卡因，导致心搏停止。在 30 秒时开始机械通气和外部胸部按压。在 1 分钟时，除了 4 种额外的静脉内治疗中的 1 种（每组 5 只动物）外，动物还接受了 5 mL/kg 20%脂肪乳剂：0.9%生理盐水、2.5μg/kg 肾上腺素、10μg/kg 肾上腺素、100μg/kg 肾上腺素；均为 1 mL/kg。脂肪乳剂推注在 4 分钟时重复。在 15 分钟时获得自主循环恢复和血流动力学指标。盐水组动物在 15 分钟时还接受了高剂量肾上腺素（100μg/kg）治疗，并监测至 20 分钟。
与生理盐水对照相比，高剂量肾上腺素给药与自主循环恢复率增加有关（5 只生理盐水治疗动物中无 1 只；2.5μg/kg 肾上腺素组中无 5 只；10μg/kg 组中 3 只[P=0.167]；100μg/kg 组中 5 只[P=0.048]）。在仅接受 100μg/kg 肾上腺素的 5 只动物中有 4 只在 15 分钟时保持自发循环，但循环逐渐减少（P=0.048）；15 分钟时平均动脉血压分别为生理盐水组 12.8（SEM 2.8）mmHg、2.5μg/kg 肾上腺素组 12.0（2.5）mmHg、10μg/kg 肾上腺素组 20.6（2.7）mmHg和 100μg/kg 肾上腺素组 26.4（3.9）mmHg（P=0.008）。在接受延迟肾上腺素治疗后，盐水治疗组的 5 只动物中有 4 只出现自主循环恢复（P=0.048）。高剂量肾上腺素给药与自主循环恢复前冠状动脉灌注压的显著增加有关。
肾上腺素似乎是自主循环恢复所必需的，但随后与这种兔布比卡因引起的心脏骤停模型中的血流动力学变量下降有关。需要进一步研究以确定肾上腺素在局部麻醉药引起的心脏骤停的脂肪乳剂复苏中的作用。
