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高血钾最早发现于未经治疗的糖尿病酮症酸中毒患者。有报道22％～32％的糖尿病酮症酸中毒者钾浓度高于6.0～6.1mmol/l,严重高血钾是导致糖尿病酮症酸中毒死亡的主要原因。 对血钾浓度升高一般解释为代谢性酸中毒时氢离子进入细胞内置换出钾离子。然而近期的研究对这些观点表示怀疑。首先,给没有糖尿病的动物静脉内注入酮酸、3—羟丁酸和其他有机酸乳酸、甲基丙二酸)并不会产生高血钾,而注入无机酸(氯化铵、盐酸)造成同等程度酸血症时可出现血钾升高。根据临床上比较这两种不同的酸,发现继发于肺水肿或酒精性酮症的乳酸性酸中毒常不会发生高钾血症。还有,一些研究认为,糖尿病酮症酸中毒时,血PH与血清钾无相关性。对此的一种解释为“由于K~+转移到缺乏缓冲的部位”,其理论基础为无机酸没有能力穿透细胞膜而进入细胞内,因此引起明显的细胞外酸中毒。
Hyperkalemia was first found in untreated diabetic ketoacidosis patients. It has been reported 22% to 32% of diabetic ketoacidosis potassium concentration higher than 6.0 ~ 6.1mmol / l, severe hyperkalemia is the leading cause of death of diabetic ketoacidosis. On the general increase in serum potassium concentration is interpreted as metabolic acidosis hydrogen ions into the cell for potassium ion replacement. However, recent studies doubt these views. First, intravenous infusion of keto acid, 3-hydroxybutyrate, and other organic acids, such as methylmalonic acid, to animals without diabetes did not produce hyperkalemia, but infusions of inorganic acids (ammonium chloride, hydrochloric acid) The same degree of acidosis may appear elevated serum potassium. According to the clinical comparison of these two different acids, hyperlipidemia is often not found in lactic acidosis secondary to pulmonary edema or alcoholic ketosis. Also, some studies suggest that diabetic ketoacidosis, blood PH and serum potassium was not related. One explanation for this is that “due to the transfer of K ~ + to a non-buffering site”, the rationale is that inorganic acids do not have the ability to penetrate the cell membrane and enter the cell, thus causing significant extracellular acidosis.