Vukmir R B, Bircher N G, Radovsky A, Safar P
Safar Center for Resuscitation Research, Pittsburgh, PA.
Crit Care Med. 1995 Mar;23(3):515-22. doi: 10.1097/00003246-199503000-00017.
Despite the absence of outcome evaluation, the use of sodium bicarbonate in cardiac arrest has declined based on advanced cardiac life-support guidelines. The effects of bicarbonate therapy on outcome in a canine model of ventricular fibrillation cardiac arrest of brief (5-min) and prolonged (15-min) duration were examined.
Prospective, randomized, controlled trial.
Experimental animal laboratory in a university medical center.
Thirty-two adult dogs, weighing 10 to 17 kg.
The animals were prepared with ketamine, nitrous oxide/oxygen, halothane, and pancuronium. Ventricular fibrillation was then electrically induced and maintained in arrest for 5 mins (n = 12) or 15 mins (n = 20). Canine advanced cardiac life-support protocols were instituted, including defibrillation, cardiopulmonary resuscitation (CPR), and the administration of epinephrine (0.1 mg/kg), atropine, and lidocaine. The bicarbonate group received 1 mmol/kg of sodium bicarbonate initially, and base deficit was corrected to -5 mmol/L with additional bicarbonate, whereas acidemia was untreated in the control group. Cardiopulmonary values were recorded at intervals between 5 mins and 24 hrs, and the neurologic deficit score was determined at 24 hrs after CPR.
The treatment group received an additional 2 to 3 mmol/kg of bicarbonate in the early postresuscitation phase. Compared with controls, the bicarbonate group demonstrated equivalent (with brief arrest) or improved (with prolonged arrest) return of spontaneous circulation and survival to 24 hrs, with lessened neurologic deficit. The acidosis of arrest was decreased in the prolonged arrest group without hypercarbia. Improved coronary and systemic perfusion pressures were noted in the bicarbonate group with prolonged arrest, and the epinephrine requirement for return of spontaneous circulation was decreased.
The empirical administration of bicarbonate improves the survival rate and neurologic outcome in a canine model of cardiac arrest.
尽管缺乏结局评估，但基于高级心脏生命支持指南，心脏骤停时碳酸氢钠的使用已有所减少。本研究考察了碳酸氢盐治疗对犬类室颤性心脏骤停（持续时间为短暂的5分钟和延长的15分钟）结局的影响。
前瞻性、随机、对照试验。
大学医学中心的实验动物实验室。
32只成年犬，体重10至17千克。
动物用氯胺酮、氧化亚氮/氧气、氟烷和泮库溴铵进行预处理。然后电诱发室颤并维持心脏骤停5分钟（n = 12）或15分钟（n = 20）。实施犬类高级心脏生命支持方案，包括除颤、心肺复苏（CPR）以及给予肾上腺素（0.1毫克/千克）、阿托品和利多卡因。碳酸氢盐组最初给予1毫摩尔/千克的碳酸氢钠，并通过额外的碳酸氢钠将碱缺失纠正至-5毫摩尔/升，而对照组则不治疗酸血症。在5分钟至24小时之间间隔记录心肺参数，并在心肺复苏后24小时测定神经功能缺损评分。
治疗组在复苏后早期额外接受了2至3毫摩尔/千克的碳酸氢盐。与对照组相比，碳酸氢盐组在短暂心脏骤停时自发循环恢复情况相当，在延长心脏骤停时自发循环恢复情况改善，且存活至24小时，神经功能缺损减轻。在延长心脏骤停组中，无高碳酸血症时心脏骤停的酸中毒情况有所减轻。在延长心脏骤停的碳酸氢盐组中，观察到冠状动脉和全身灌注压有所改善，且恢复自发循环所需的肾上腺素剂量减少。
在犬类心脏骤停模型中，经验性给予碳酸氢盐可提高生存率和神经功能结局。
