The Department of Emergency Medicine, Chonnam National University Hospital, Gwangju, Republic of Korea.
Acad Emerg Med. 2014 Apr;21(4):392-400. doi: 10.1111/acem.12348.
Several studies in patients who underwent open heart surgery found that myocardial ischemic damage was reduced by potassium cardioplegia combined with lidocaine infusion. The authors evaluated the effects of potassium/lidocaine-induced cardiac standstill during conventional cardiopulmonary resuscitation (CPR) on myocardial injury and left ventricular dysfunction after resuscitation from prolonged ventricular fibrillation (VF) cardiac arrest in a pig model.
Ventricular fibrillation was induced in 16 pigs, and circulatory arrest was maintained for 14 minutes. Animals were then resuscitated by standard CPR. Animals were randomized at the start of CPR to receive 20 mL of saline (control group) or 0.9 mEq/kg potassium chloride and 1.2 mg/kg lidocaine diluted to 20 mL (K-lido group).
Seven animals in each group achieved return of spontaneous circulation (ROSC; p=1.000). Four of the K-lido group animals (50%) achieved ROSC without countershock. Resuscitated animals in the K-lido group required fewer countershocks (p=0.004), smaller doses of epinephrine (p=0.009), and shorter durations of CPR (p=0.004) than did the control group. The uncorrected troponin-I at 4 hours after ROSC was lower in the K-lido group compared with the control group (2.82 ng/mL, 95% confidence interval [CI]=1.07 to 3.38 ng/mL vs. 6.55 ng/mL, 95% CI=4.84 to 13.30 ng/mL; p=0.025), although the difference was not significant after Bonferroni correction. The magnitude of reduction in left ventricular ejection fraction (LVEF) between baseline and 1 hour after ROSC was significantly lower in the K-lido group (26.5%, SD±6.1% vs. 39.1%, SD±6.8%; p=0.004).
In a pig model of untreated VF cardiac arrest for 14 minutes, resuscitation with potassium/lidocaine-induced cardiac standstill during conventional CPR tended to reduce myocardial injury and decreased the severity of postresuscitation myocardial dysfunction significantly.
几项针对接受心脏直视手术患者的研究发现，钾心脏停搏联合利多卡因输注可减少心肌缺血损伤。作者评估了在猪模型中，常规心肺复苏（CPR）期间钾/利多卡因诱导的心脏停搏对长时间室颤（VF）心脏骤停后心肌损伤和左心室功能障碍的影响。
在 16 头猪中诱发 VF，并维持循环停止 14 分钟。然后通过标准 CPR 对动物进行复苏。在 CPR 开始时，动物被随机分配接受 20 mL 生理盐水（对照组）或 0.9 mEq/kg 氯化钾和 1.2 mg/kg 利多卡因稀释至 20 mL（K-lido 组）。
每组有 7 只动物恢复自主循环（ROSC；p=1.000）。K-lido 组有 4 只动物（50%）无需除颤即可实现 ROSC。K-lido 组复苏动物需要更少的除颤（p=0.004）、更小剂量的肾上腺素（p=0.009）和更短的 CPR 持续时间（p=0.004），与对照组相比。ROSC 后 4 小时未校正的肌钙蛋白 I 在 K-lido 组低于对照组（2.82ng/mL，95%置信区间[CI]：1.07 至 3.38ng/mL 与 6.55ng/mL，95%CI：4.84 至 13.30ng/mL；p=0.025），尽管经过 Bonferroni 校正后差异无统计学意义。K-lido 组在 ROSC 后 1 小时与基线相比左心室射血分数（LVEF）的降低幅度明显较小（26.5%，标准差±6.1%与 39.1%，标准差±6.8%；p=0.004）。
在 14 分钟未经治疗的 VF 心脏骤停的猪模型中，常规 CPR 期间钾/利多卡因诱导的心脏停搏复苏可降低心肌损伤并显著减轻复苏后心肌功能障碍的严重程度。
