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首页> 外文期刊>Heart and Lung: The Journal of Critical Care >Life-threatening hypokalemia following rapid correction of respiratory acidosis
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Life-threatening hypokalemia following rapid correction of respiratory acidosis

机译:快速纠正呼吸性酸中毒威胁生命的低钾血症

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摘要

A 56-year-old woman with a history of paraplegia and chronic pain due to neuromyelitis optica (Devic's syndrome) was admitted to a spinal cord injury unit for management of a sacral decubitus ulcer. During the hospitalization, she required emergency transfer to the intensive care unit (ICU) because of progressive deterioration of respiratory muscle function, severe respiratory acidosis, obtundation and hypotension. Upon transfer to the ICU, arterial blood gas revealed severe acute-on-chronic respiratory acidosis (pH 7.00, PCO2 120mmHg, PO2 211mmHg). The patient was immediately intubated and mechanically ventilated. Intravenous fluid boluses of normal saline (10.5L in about 24h) and vasopressors were started with rapid correction of hypotension. In addition, she was given hydrocortisone. Within 40min of initiation of mechanical ventilation, there was improvement in acute respiratory acidosis. Sixteen hours later, however, the patient developed life-threatening hypokalemia (K+ of 2.1mEq/L) and hypomagnesemia (Mg of 1.4mg/dL). Despite aggressive potassium supplementation, hypokalemia continued to worsen over the next several hours (K+ of 1.7mEq/L). Urine studies revealed renal potassium wasting. We reason that the recalcitrant life-threatening hypokalemia was caused by several mechanisms including total body potassium depletion (chronic respiratory acidosis), a shift of potassium from the extracellular to intracellular space (rapid correction of respiratory acidosis with mechanical ventilation), increased sodium delivery to the distal nephron (normal saline resuscitation), hyperaldosteronism (secondary to hypotension plus administration of hydrocortisone) and hypomagnesemia. We conclude that rapid correction of respiratory acidosis, especially in the setting of hypotension, can lead to life-threatening hypokalemia. Serum potassium levels must be monitored closely in these patients, as failure to do so can lead to potentially lethal consequences.
机译:一名56岁的女性因视神经脊髓炎(德维克氏综合症)而患有截瘫和慢性疼痛史,被送进脊髓损伤科治疗for部褥疮。在住院期间,由于呼吸肌功能的逐步恶化,严重的呼吸性酸中毒,充血和低血压,她需要紧急转移到重症监护病房(ICU)。转移至ICU后,动脉血气显示出严重的慢性呼吸性酸中毒(pH 7.00,PCO2 120mmHg,PO2 211mmHg)。立即给患者插管并进行机械通气。静脉注射大剂量生理盐水(约24h时为10.5L)和升压药,以迅速纠正低血压。此外,她还接受了氢化可的松治疗。机械通气开始后40分钟内,急性呼吸性酸中毒有所改善。然而,十六小时后,患者出现了危及生命的低钾血症(K +为2.1mEq / L)和低镁血症(镁为1.4mg / dL)。尽管积极补充钾,低钾血症在接下来的几个小时内仍继续恶化(K +为1.7mEq / L)。尿液研究显示肾脏钾盐浪费。我们认为,顽固性致命性低钾血症是由多种机制引起的,这些机制包括全身钾耗竭(慢性呼吸性酸中毒),钾从细胞外空间转移到细胞内空间(通过机械通气快速纠正呼吸性酸中毒),增加的钠传递至远端肾单位(生理盐水复苏正常),醛固酮增多症(继发于低血压,低血压加氢化可的松)和低镁血症。我们得出的结论是,呼吸性酸中毒的快速纠正,尤其是在低血压的情况下,可能导致危及生命的低钾血症。这些患者的血清钾水平必须严密监测,否则可能会导致致命的后果。

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