Bar-Joseph G, Weinberger T, Castel T, Bar-Joseph N, Laor A, Bursztein S, Ben Haim S
Pediatric Intensive Care Unit, Rambam Medical Center, Haifa, Israel.
Crit Care Med. 1998 Aug;26(8):1397-408. doi: 10.1097/00003246-199808000-00027.
During cardiopulmonary resuscitation (CPR), elimination of CO2 was shown to be limited by low tissue perfusion, especially when very low perfusion pressures were generated. It has therefore been suggested that sodium bicarbonate (NaHCO3), by producing CO2, might aggravate the hypercarbic component of the existing acidosis and thereby worsen CPR outcome. The objectives of this study were to evaluate the effects of CO2 producing and non-CO2 producing buffers in a canine model of prolonged ventricular fibrillation followed by effective CPR.
Prospective, randomized, controlled, blinded trial.
Experimental animal research laboratory in a university research center.
Thirty-eight adult dogs, weighing 20 to 35 kg.
Animals were prepared for study with thiopental followed by halothane, diazepam, and pancuronium. Ventricular fibrillation was electrically induced, and after 10 mins, CPR was initiated, including ventilation with an FIO2 of 1.0, manual chest compressions, administration of epinephrine (0.1 mg/kg every 5 mins), and defibrillation. A dose of buffer, equivalent to 1 mmol/kg of NaHCO3, was administered every 10 mins from start of CPR. Animals were randomized to receive either NaHCO3, Carbicarb, THAM, or 0.9% sodium chloride (NaCl). CPR was continued for up to 40 mins or until return of spontaneous circulation.
Buffer-treated animals had a higher resuscitability rate compared with NaCl controls. Spontaneous circulation returned earlier and at a significantly higher rate after NaHCO3 (in seven of nine dogs), and after Carbicarb (six of ten dogs) compared with NaCl controls (two of ten dogs). Spontaneous circulation was achieved twice as fast after NaHCO3 compared with NaCl (14.6 vs. 28 mins, respectively). Hydrogen ion (H+) concentration and base excess, obtained 2 mins after the first buffer dose, were the best predictors of resuscitability. Arterial and mixed venous Pco2 did not increase after NaHCO3 or Carbicarb compared with NaCl.
Buffer therapy promotes successful resuscitation after prolonged cardiac arrest, regardless of coronary perfusion pressure. NaHCO3, and to a lesser degree, Carbicarb, are beneficial in promoting early return of spontaneous circulation. When epinephrine is used to promote tissue perfusion, there is no evidence for hypercarbic venous acidosis associated with the use of these CO2 generating buffers.
在心肺复苏(CPR)期间,二氧化碳(CO2)的清除被证明受低组织灌注限制,尤其是当产生极低灌注压时。因此,有人提出碳酸氢钠(NaHCO3)通过产生CO2,可能会加重现有酸中毒的高碳酸血症成分,从而恶化心肺复苏结果。本研究的目的是评估在犬类长时间室颤后进行有效心肺复苏的模型中,产生CO2和不产生CO2的缓冲液的效果。
前瞻性、随机、对照、盲法试验。
大学研究中心的实验动物研究实验室。
38只成年犬,体重20至35千克。
动物用硫喷妥钠麻醉,随后用氟烷、地西泮和泮库溴铵。通过电诱导室颤,10分钟后开始心肺复苏,包括用1.0的吸入氧分数(FIO2)通气、手动胸外按压、给予肾上腺素(每5分钟0.1毫克/千克)和除颤。从心肺复苏开始每10分钟给予一剂相当于1毫摩尔/千克NaHCO3的缓冲液。动物被随机分为接受NaHCO3、卡比多巴(Carbicarb)、三羟甲基氨基甲烷(THAM)或0.9%氯化钠(NaCl)。心肺复苏持续40分钟或直至自主循环恢复。
与NaCl对照组相比,接受缓冲液治疗的动物复苏成功率更高。与NaCl对照组(10只中有2只)相比,NaHCO3组(9只中有7只)和卡比多巴组(10只中有6只)自主循环恢复更早且比例显著更高。与NaCl组相比,NaHCO3组自主循环恢复速度快两倍(分别为14.6分钟和28分钟)。首次给予缓冲液后2分钟测得的氢离子(H+)浓度和碱剩余是复苏成功率的最佳预测指标。与NaCl组相比,NaHCO3组或卡比多巴组后动脉血和混合静脉血二氧化碳分压(Pco2)没有升高。
缓冲液治疗可促进长时间心脏骤停后的成功复苏,无论冠状动脉灌注压如何。NaHCO3以及程度较轻的卡比多巴有利于促进自主循环的早期恢复。当使用肾上腺素促进组织灌注时,没有证据表明使用这些产生CO2的缓冲液会导致高碳酸血症性静脉酸中毒。