Christensen Toke Folke, Baekgaard Martin, Dideriksen Jacob Lund, Steimle Kristoffer Lindegaard, Mogensen Mads Lause, Kildegaard Jonas, Struijk Johannes Jan, Hejlesen Ole Kristian
Department of Health Science and Technology, Aalborg University, Aalborg, Denmark.
J Diabetes Sci Technol. 2009 Jul 1;3(4):887-94. doi: 10.1177/193229680900300436.
Adrenaline release and excess insulin during hypoglycemia stimulate the uptake of potassium from the bloodstream, causing low plasma potassium (hypokalemia). Hypokalemia has a profound effect on the heart and is associated with an increased risk of malignant cardiac arrhythmias. It is the aim of this study to develop a physiological model of potassium changes during hypoglycemia to better understand the effect of hypoglycemia on plasma potassium.
Potassium counterregulation to hypokalemia was modeled as a linear function dependent on the absolute potassium level. An insulin-induced uptake of potassium was modeled using a negative exponential function, and an adrenaline-induced uptake of potassium was modeled as a linear function. Functional expressions for the three components were found using published data.
The performance of the model was evaluated by simulating plasma potassium from three published studies. Simulations were done using measured levels of adrenaline and insulin. The mean root mean squared error (RMSE) of simulating plasma potassium from the three studies was 0.09 mmol/liter, and the mean normalized RMSE was 14%. The mean difference between nadirs in simulated and measured potassium was 0.12 mmol/liter.
The presented model simulated plasma potassium with good accuracy in a wide range of clinical settings. The limited number of hypoglycemic episodes in the test set necessitates further tests to substantiate the ability of the model to simulate potassium during hypoglycemia. In conclusion, the model is a good first step toward better understanding of changes in plasma potassium during hypoglycemia.
低血糖期间肾上腺素释放和胰岛素过量会刺激钾从血液中摄取,导致血浆钾水平降低(低钾血症)。低钾血症对心脏有深远影响,并与恶性心律失常风险增加有关。本研究的目的是建立低血糖期间钾变化的生理模型,以更好地理解低血糖对血浆钾的影响。
将对低钾血症的钾代偿调节模拟为依赖于绝对钾水平的线性函数。使用负指数函数模拟胰岛素诱导的钾摄取,将肾上腺素诱导的钾摄取模拟为线性函数。利用已发表的数据找到这三个组成部分的函数表达式。
通过模拟三项已发表研究中的血浆钾来评估模型的性能。使用测量的肾上腺素和胰岛素水平进行模拟。三项研究模拟血浆钾的平均均方根误差(RMSE)为0.09毫摩尔/升,平均归一化RMSE为14%。模拟钾和测量钾最低点之间的平均差异为0.12毫摩尔/升。
所提出的模型在广泛的临床环境中能准确模拟血浆钾。测试集中低血糖发作次数有限,需要进一步测试以证实该模型在低血糖期间模拟钾的能力。总之,该模型是朝着更好地理解低血糖期间血浆钾变化迈出的良好第一步。