Knight R K, Miall P A, Hawkins L A, Dacombe J, Edwards C R, Hamer J
Br Heart J. 1979 Sep;42(3):316-25. doi: 10.1136/hrt.42.3.316.
To assess the relation of hyperaldosteronism and potassium depletion to the intensity of diuretic therapy we have measured plasma aldosterone by radioimmunoassay and total exchangeable potassium by radioisotope dilution in 24 patients when they were stable at the end of their preparation for cardiac operation. Some patients required intensive frusemide therapy to reach an optimal state for operation and many showed hyperaldosteronism. Plasma aldosterone was significantly related to daily dose of frusemide (r=0.77). Depletion of total exchangeable potassium expressed in terms of predicted weight was significantly related to plasma aldosterone (r= -0.64). The reduction in total exchangeable potassium is interpreted as chiefly related to loss of lean tissue mass from the wasting that leads to cardiac cachexia, but evidence is presented on the basis of measurements of extracellular fluid volume as sulphate space (20 patients) of entry of sodium into the cells which may indicate a true cellular potassium loss. Although plasma potassium is usually easily maintained with oral potassium supplements or aldosterone antagonists, we postulate that intensive diuretic therapy in severe heart disease may provoke hyperaldosteronism which accentuates potassium loss and may contribute to wasting and to intracellular potassium depletion in critical tissue, such as myocardium.
为了评估醛固酮增多症和钾缺乏与利尿剂治疗强度之间的关系,我们在24例患者心脏手术准备结束病情稳定时,通过放射免疫分析法测定了血浆醛固酮,并通过放射性同位素稀释法测定了可交换钾总量。一些患者需要大剂量速尿治疗才能达到最佳手术状态,许多患者表现出醛固酮增多症。血浆醛固酮与速尿日剂量显著相关(r = 0.77)。以预测体重表示的可交换钾总量的减少与血浆醛固酮显著相关(r = -0.64)。可交换钾总量的减少主要被解释为与导致心脏恶病质的消瘦引起的瘦组织量减少有关,但基于作为硫酸盐空间的细胞外液量测量结果(20例患者)以及钠进入细胞的情况,有证据表明可能存在真正的细胞内钾丢失。尽管通过口服钾补充剂或醛固酮拮抗剂通常很容易维持血浆钾水平,但我们推测,重症心脏病患者的强化利尿剂治疗可能会引发醛固酮增多症,从而加重钾丢失,并可能导致消瘦以及关键组织(如心肌)的细胞内钾缺乏。