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心搏骤停前无酸碱及电解质紊乱病因及证据之患者22例,自主循环恢复后3小时内有低血钾者12例(54.5%),低血钠2例(9%)。低血钾组之pHa为7.266±0.045,正常血钾组为7.294±0.048(P>0.05)、无1例有碱中毒表现。血钾浓度与复苏时肾上腺素用量及恢复自主循环(ROSC)时间长短之间无直线相关(r分别为0.139及0.168),提示复苏后低血钾并非碱中毒引起,它与外源性使用肾上腺素也无关。作者认为复苏后早期低血钾可能系复苏时机体内源性肾上腺素释放增加使K+再分布进入细胞内所致。低血钾组与正常血钾组之CPCR成功率无显著性差异(58.3%对50%,P>0.05),提示复苏后低血钾与随后之死亡的死亡率无关。严重低血钾(<0.3mEq/L)患者,尤其是原有心脏病者,因有严重心律失常甚至再发室颤之可能,应引起重视。
Twenty-two patients (54.5%) had hyponatremia and 2 (9%) had hyponatremia within 3 hours after spontaneous circulation had recovered after elective cardiac arrest without etiology and evidence of acid-base and electrolyte disturbances. The pH value of hypokalemia group was 7.266 ± 0.045, and that of normal potassium group was 7.294 ± 0.048 (P> 0.05). No one had alkalosis. There was no linear correlation between serum potassium levels and the amount of epinephrine during resuscitation and the duration of ROSC (r = 0.139 and 0.168, respectively), suggesting that hypokalemia is not caused by alkalosis after resuscitation. It is associated with exogenous adrenal There is nothing to do with prime. The authors suggest that early post-recovery hypokalemia may be due to an increase in endogenous adrenergic release that redistributes K + into the cell during resuscitation. There was no significant difference in the success rate of CPCR between hypokalemia and normal potassium groups (58.3% vs 50%, P> 0.05), suggesting that hypokalemia after resuscitation has no relation with subsequent mortality. Severe hypokalemia (<0.3mEq / L) patients, especially those with heart disease, due to severe arrhythmia and even the possibility of recurrent atrial fibrillation, should pay attention.