Schaefer M, Link J, Hannemann L, Rudolph K H
Department of Anesthesiology and Intensive Care Medicine, Universitätsklinikum Benjamin Franklin, Berlin, Germany.
Intensive Care Med. 1995 Mar;21(3):235-7. doi: 10.1007/BF01701479.
A sudden decrease of serum potassium below 2.5 mmol/l carries the risk of dangerous arrhythmias and requires immediate replacement therapy [6]. We refer to a patient with a brain stem compression after head injury, who developed a profound hypokalemia (K+ = 1.2 mmol/l) with life-threatening arrhythmias, probably due to a catecholamine induced intracellular potassium shift (beta-2-stimulation). Only by aggressive potassium replacement up to 80 mmol/h (610 mmol/16 h) could potassium levels be increased and cardiac arrhythmias terminated. Although replacement therapy was stopped when the serum K(+)-level increased to 2.4 mmol/l, 3.5 h later the patient became hyperkalemic (8.1 mmol/l). This was probably due to a secondary shift of potassium from intra- to extracellular space. In patients with severe head trauma and the potential risk of excessive catecholamine release special attention must be paid to changes in potassium balance.
血清钾突然降至2.5 mmol/l以下会有发生危险心律失常的风险，需要立即进行补充治疗[6]。我们报告一名头部受伤后出现脑干受压的患者，该患者出现了严重低钾血症（血钾 = 1.2 mmol/l），伴有危及生命的心律失常，这可能是由于儿茶酚胺诱导的细胞内钾转移（β-2刺激）所致。只有通过高达80 mmol/h（610 mmol/16 h）的积极补钾，血钾水平才能升高，心律失常才能终止。尽管当血清钾水平升至2.4 mmol/l时停止了补充治疗，但3.5小时后患者出现了高钾血症（8.1 mmol/l）。这可能是由于钾从细胞内空间向细胞外空间的继发性转移所致。对于有严重头部创伤且有儿茶酚胺过度释放潜在风险的患者，必须特别关注钾平衡的变化。
