氯化钙治疗猪模型急性地高辛中毒引起的高钾血症的效果。

Jason B Hack, Jonathan H Woody, Daniel E Lewis, Kori Brewer, William J Meggs
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引用次数: 28

摘要

背景:静脉(IV)钙治疗地高辛中毒引起的高钾血症被认为是有潜在危险的,根据大量较早的文献,总的来说,钙治疗增加了心糖苷毒性(心律失常增加,死亡率更高)。目的:本初步研究旨在确定与生理盐水相比,氯化钙给药是否会影响高钾血症、地高辛中毒猪的死亡时间。方法:确定0.25 mg/kg的地高辛IV为适宜毒性。当出现与高钾血症一致的心律失常时,给予IV氯化钙(CaCl)丸(10 mg/kg,组1,n=6)或等量生理盐水(组2,n=6)。观察三个时间间隔:时间间隔1:从地高辛给药(T0)到ECG变化与高钾血症发生一致的时间间隔(此时给予氯化钙或生理盐水);时间间隔2:从出现符合高钾血症的心电图变化到心脏停止的时间间隔;时间间隔3:地高辛给药至心脏停止的时间间隔。监测两组患者的心律变化、血清钾水平和心脏骤停时间。结果:0.25 mg/kg地高辛静脉给药约1小时后引起高钾血症、心律失常和死亡。组1:区间1平均18.75 (sd +/-7.96) min,区间2平均16.75 (sd +/-17.17) min,区间3平均35.5 (sd +/-14.49) min;组2:间隔1平均24.8 (sd +/-4.71) min,间隔2平均19.5 (sd +/-15.92) min,间隔3平均44.3 (sd +/-13.80) min。各组间在时间间隔1 (p=0.43)、时间间隔2 (p=0.65)、时间间隔3 (p=0.40)均无统计学差异。在整个研究期间,血清钾没有差异。结论:在急性地高辛中毒致高钾血症的情况下,静脉注射氯化钙对死亡率和死亡时间没有影响。
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The effect of calcium chloride in treating hyperkalemia due to acute digoxin toxicity in a porcine model.

Background: The administration of intravenous (IV) calcium to treat hyperkalemia resulting from digoxin poisoning is considered potentially dangerous, based on a body of older literature which, in sum, reported increased cardiac glycoside toxicity with calcium administration (increased arrhythmias, higher rate of death).

Objective: This pilot study sought to determine if the administration of calcium chloride when compared to normal saline would affect time to death when given to hyperkalemic, digoxin toxic swine.

Methods: Digoxin IV at 0.25 mg/kg was determined to be appropriately toxic for this study. When arrhythmias consistent with hyperkalemia developed, animals were given either IV calcium chloride (CaCl) bolus (10 mg/kg, Group 1, n=6) or normal saline volume equivalent (Group 2, n=6). Three intervals were observed: Interval 1: time interval from digoxin administration (T0) to when ECG changes consistent with hyperkalemia developed (at which point calcium chloride or normal saline was administered); Interval 2: time interval from the development of ECG changes consistent with hyperkalemia to asystole; Interval 3: time interval from digoxin administration to asystole. Both groups were monitored for changes in heart rhythms, serum potassium levels, and time to asystole.

Results: The intravenous digoxin dose of 0.25 mg/kg induced hyperkalemia, arrhythmias, and death approximately 1 h after administration in all animals studied. Group 1: Interval 1 averaged 18.75 (S.D. +/-7.96) min, Interval 2 averaged 16.75 (S.D. +/-17.17) min, and Interval 3 averaged 35.5 (S.D. +/-14.49) min range; Group 2: average Interval 1 24.8 (S.D. +/-4.71) min, Interval 2 averaged 19.5 (S.D.+/-15.92), Interval 3 averaged 44.3 (S.D. +/-13.80) minutes. There was no statistically significant difference between the groups at any time interval, Interval 1 (p=0.43), Interval 2 (p=0.65), Interval 3 (p=0.40). There was no difference in serum potassium throughout the study period.

Conclusion: The administration of intravenous CaCl in the setting of hyperkalemia from acute digoxin toxicity did not affect mortality or time to death at the dose administered.

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