Michaeli J, Bassan M M, Brezis M
J Electrocardiol. 1986 Oct;19(4):393-6. doi: 10.1016/s0022-0736(86)81068-8.
An 83-year-old woman was hospitalized with complete atrioventricular block and a pulse of 20/min. Three days earlier an electrocardiogram had revealed right bundle branch block with classic type II second degree atrioventricular block. Admission potassium was 7.8 meq/L; within 24 hours the potassium was lowered to 4.9 meq/L and the atrioventricular block disappeared. The patient was followed for nineteen months and remained normokalemic without recurrence of atrioventricular block, although the right bundle branch block persisted. She was then readmitted with bradycardia due to complete atrioventricular block despite normokalemia. We conclude that hyperkalemia can produce the classic picture of progressive bilateral bundle branch disease leading to high degree atrioventricular block, although this seems to occur in patients with extensive intrinsic disease of the conduction system.
一名83岁女性因完全性房室传导阻滞和脉搏20次/分钟入院。三天前心电图显示右束支传导阻滞合并典型II型二度房室传导阻滞。入院时血钾为7.8毫当量/升;24小时内血钾降至4.9毫当量/升,房室传导阻滞消失。对该患者随访19个月,血钾保持正常,房室传导阻滞未复发,尽管右束支传导阻滞仍然存在。之后她因血钾正常但出现完全性房室传导阻滞导致的心动过缓再次入院。我们得出结论,高钾血症可导致典型的进行性双侧束支疾病表现,进而导致高度房室传导阻滞,尽管这种情况似乎发生在传导系统存在广泛内在疾病的患者中。