Salerno D M, Katz A, Dunbar D N, Fjeldos-Sperbeck K
Department of Medicine, Hennepin County Medical Center, University of Minnesota, Minneapolis.
Pacing Clin Electrophysiol. 1993 Sep;16(9):1862-71. doi: 10.1111/j.1540-8159.1993.tb01821.x.
We have observed hypokalemia after cardioversion from spontaneous out-of-hospital ventricular fibrillation and induced ventricular tachycardia. To test the hypothesis that the hormone response to the hemodynamic stress of the arrhythmia initiated the change in potassium, we compared the electrolytes and hormones in three groups of patients. We observed a decrease in serum potassium and magnesium after cardioversion from ventricular tachycardia induced by programmed stimulation, but not after normal programmed stimulation of the ventricle or after cardioversion from stable atrial fibrillation. These changes were preceded first by a rise in norepinephrine and epinephrine, then a rise in glucose, followed by a rise in insulin. The stimulus for these changes was probably the hypotension associated with ventricular tachycardia. The sequence of changes suggests that the decrease of potassium and magnesium after ventricular tachycardia was due to a shift of the electrolytes into cells, related to the insulin-mediated movement of glucose from the blood into cells.
我们观察到,在院外自发性心室颤动及诱发的室性心动过速复律后出现了低钾血症。为了验证心律失常的血流动力学应激引发激素反应进而导致钾变化这一假说,我们比较了三组患者的电解质和激素情况。我们观察到,经程序刺激诱发的室性心动过速复律后,血清钾和镁水平降低,但在心室正常程序刺激后或稳定型心房颤动复律后未出现这种情况。这些变化首先是去甲肾上腺素和肾上腺素升高,然后是血糖升高,接着是胰岛素升高。这些变化的刺激因素可能是与室性心动过速相关的低血压。变化顺序表明,室性心动过速后钾和镁的降低是由于电解质向细胞内转移,这与胰岛素介导的葡萄糖从血液进入细胞的过程有关。